Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3156_Библиотеки_им_академика_М_И_Перельмана.pdf
REFERENCES
1. Boongird S, Shah N, Nolin TD, Unruh ML. Nocturia and aging: diagnosis and treatment. Adv Chronic
Kidney Dis 2010;17(4):e27–e40.
2. Jin MH, Moon du G. Practical management of nocturia in urology. Indian J Urol 2008;24(3):
289–294.
3. Pressman MR, Figueroa WG, Kendrick-Mohamed J, Greenspon LW, Peterson DD. Nocturia.
A rarely recognized symptom of sleep apnea and other occult sleep disorders. Arch Intern Med
1996;156(5):545–550.
10.6
I. BACKGROUND
A. Oliguria is defined as urine volume less than 400 mL/d or less than 0.5 mL/kg/h over a
6-hour period in adults and children and less than 1 mL/kg/h in infants (1, 2). While
anuria is defined as the total absence of urine, in the clinical setting, a patient with a
urine output of less than 50–100 mL/24 h is considered to be anuric. The presence of
oliguria signifies a renal insult that has led to a marked decrease in the glomerular filtra-
tion rate (GFR), causing increased urea and creatinine levels and subsequent water and
sodium retention. While oliguria is typically one of the earliest manifestations of acute
kidney injury (AKI), it often occurs before changes in serum creatinine. However, not
all patients with AKI demonstrate oliguria.
B. Patients presenting to the office setting with acute oliguria should be hospitalized due
to the risk of developing potentially fatal complications such as hyperkalemia (mani-
fested by weakness or paralysis and electrocardiogram changes), fluid overload, meta-
bolic acidosis, and pericarditis (1). Fortunately, the prognosis of oliguria that develops
outside the hospital is typically good if treated early as it is typically due to one cause
(3): dehydration. Hospital-acquired oliguria and AKI, however, carry a worse progno-
sis because the cause is often multifactorial leading to more severe and permanent renal
injury (4).
II. PATHOPHYSIOLOGY
A. Oliguria.
The cause of oliguria is (1) prerenal, (2) renal (intrinsic), or (3) postrenal (see
Table 10.6.1).
1. Prerenal causes are due to renal hypoperfusion resulting in a decrease in GFR. Often,
renal function recovers with prompt treatment of the underlying cause (5).
2. Renal disorders are characterized by structural damage to the kidney parenchyma itself
and are categorized based on the location of injury. The most common cause of renal
AKI is acute tubular necrosis, which is typically due to ischemia or nephrotoxins.
3. Postrenal disorders are a result of obstruction in the urinary tract anywhere from the renal
pelvis down to the urethra. In order to develop oliguria, however, upper tract obstruction
must be bilateral or occur in patients with a solitary kidney. The absence of oliguria does
not rule out partial or intermittent obstruction; these patients often have normal or even
elevated urine output (6). In children, congenital ureteral or urethral strictures or valves
predominate as a cause of obstruction while malignancy, benign prostatic hypertrophy,
and calculi are the most common causes of obstructive uropathy in adults (5).
B. Anuria is most commonly a result of complete bilateral urinary tract obstruction or
shock. Other more rare causes of anuria include hemolytic uremic syndrome, bilat-
eral renal cortical necrosis, bilateral renal arterial or venous obstruction, and rapidly
Oliguria and
A
nuria
Deepa J. Borde and George P. Samraj
228
TABLE 10.6.1 Causes of Acute Oliguria
Prerenal Renal Postrenal
Hypovolemia
Hemorrhage
GI loss (including nasogastric
suction)
Diuretics
Glucosuria
Cutaneous loss (burns or
sweat)
Third spacing (burns,
peritonitis, pancreatitis,
trauma)
Acute GN
Postinfectious GN
Endocarditis-associated GN
Systemic vasculitis
Rapidly progressive GN
Membranoproliferative GN
Mesangial proliferative GN
IgA nephropathy
Upper tract obstruction
Intrinsic
Nephrolithiasis
Papillary necrosis
Blood clots
Malignancy
Extrinsic
Retroperitoneal fibrosis
Malignancy
Endometriosis
AAA
Decreased effective blood
volume
Sepsis
Congestive heart failure
Cirrhosis
Nephrotic syndrome
Vasodilatory drugs
Anaphylaxis
Anesthetic drugs
Acute interstitial nephritis
Drug-induced (penicillins,
cephalosporins,
sulfonamides, rifampin,
phenytoin, furosemide, PPIs,
and NSAIDs)
Pyelonephritis
Malignancy
Lower tract obstruction
Bladder
Neurogenic bladder
TCC
Blood clots
Bladder calculus
Prostate
Prostate cancer
BPH
Urethra
Stricture
Phimosis
Urethral valves
Urinary catheter
Obstructed
Kinked
Misplaced
Decreased cardiac output
Myocardial infarction
Pulmonary embolus
Cardiac tamponade
Mechanical ventilation
Acute tubular necrosis
Ischemic (sustained prerenal
injury)
Nephrotoxic (aminoglycosides,
radiocontrast media,
hemolysis, rhabdomyolysis,
amphotericin, cisplatin,
ifosfamide, acetaminophen)
Impaired renal perfusion
ACE inhibitors
NSAIDs
Acute vascular disease
Bilateral renal artery stenosis,
thrombosis, embolism, or
dissecting aneurysm
Intrarenal vasoconstriction
Hypercalcemia
Hepatorenal
Atheroembolic disease
HELLP syndrome
Malignant hypertension
TTP
Hemolytic uremic syndrome
(Continued)
229
progressive glomerulonephritis (7). In patients with an indwelling catheter prior to the
development of anuria, catheter blockage, kinks, and malposition must be ruled out
prior to initiating an extensive workup.
III. EVALUATION
A. History.
Patients with oliguria may or may not report decreased urine output, but may
report other symptoms that can help to discern the cause of their illness.
1. Does the patient report symptoms of dehydration or bleeding that would lead to prerenal
causes of AKI? Nausea and vomiting may be present, either as a result of gastrointestinal
illness or as symptoms of uremia. Other uremic symptoms include anorexia, fatigue,
confusion, pruritus, and even seizures. Diarrhea, bleeding, dyspnea, lower extremity
edema, or diuretic use may indicate a prerenal cause of oliguria.
2. Does the patient report symptoms of voiding dysfunction or pelvic or retroperitoneal
disease pointing to an obstructive cause of oliguria?
3. Does the patient have a history of recent travel, occupational hazards, or new medica-
tions, specifically antibiotics or over-the-counter nonsteroidal anti-inflammatory drug
use that could lead to a renal cause of AKI? Does the patient have any recent exposure to
radiocontrast agents, episodes of prolonged hypotension, or angiographic studies involv-
ing the aorta?
B. Physical Examination. After review of the patient’s vital signs, including orthostatics
where indicated, the patient should be evaluated for physical signs of volume depletion
or fluid overload. A thorough abdominal exam should be performed to evaluate for
bladder distension and renal artery bruits and consideration should be given to perform-
ing a pelvic exam if a pelvic mass is suspected or rectal exam if the history indicates
prostate enlargement. A careful skin exam may reveal purpura consistent with vasculitis,
livedo reticularis indicating atheroembolic disease, or rash consistent with interstitial
nephritis.
C. Laboratory Tests
1. Urinalysis is typically normal in prerenal causes of oliguria, but hyaline and fine granular
casts may be present in the urine sediment and the specific gravity may be elevated. In
renal causes, on the other hand, examination of the urine sediment is quite useful, often
revealing brown granular casts and tubular epithelial cells in patients with acute tubular
necrosis and dysmorphic red blood cells and red cell casts in those with glomerulone-
phritis. White blood cells or casts and eosinophils are present in the urine sediment in
patients with interstitial nephritis, and crystalluria or proteinuria in those with intratu-
bular obstruction.
2. Urinary Indices. Table 10.6.2 outlines the use of urinary indices to differentiate prer-
enal, renal, and postrenal etiologies of oliguria. In prerenal AKI, the kidneys respond
TABLE 10.6.1 Causes of Acute Oliguria
Prerenal Renal Postrenal
Acute intratubular obstruction
Paraprotein (multiple myeloma)
Crystalline (ethylene glycol
ingestion, tumor lysis,
acyclovir, methotrexate)
AAA, abdominal aortic aneurysm; ACE, angiotensin-converting enzyme; BPH, benign prostatic
hypertrophy; GI, gastrointestinal; GN, glomerulonephritis; HELLP, hemolysis, elevated liver enzymes,
and low platelets; IgA, immunoglobulin A; NSAIDs, nonsteroidal anti-inflammatory drugs; PPI,
proton pump inhibitor; TCC, transitional cell carcinoma; TTP, thrombotic thrombocytopenic purpura.
(Continued)
230
to hypoperfusion by retaining sodium in order to retain water. Thus, the fractional
excretion of sodium (FENa) in prerenal causes of oliguria is typically less than 1%.
There are two main instances of prerenal AKI in which compensatory sodium reab-
sorption is impaired leading to a FENa that is greater than 1%: diuretic therapy and
chronic kidney disease patients who develop a prerenal state. In patients on diuretic
therapy, the fractional excretion of urea is a more useful measure, typically being
less than 35% (8). There are two renal causes of AKI in which the FENa is less than
1%: contrast nephropathy and pigment nephropathy (due to rhabdomyolysis or
hemolysis).
D. Diagnostic Testing. An indwelling urinary catheter is useful as a diagnostic tool, for
accurate urine volume measurement, and also for treatment in cases of lower urinary tract
obstruction. Patients suspected of having obstructive uropathy should have a bladder scan
or urinary catheter placement after voiding to obtain measurement of postvoid residual
(PVR). A PVR of greater than 100 mL is indicative of bladder outlet obstruction. Upper
tract obstruction may be evaluated with renal ultrasound or renal protocol computed
tomography. A careful intravenous fluid trial can be used as a diagnostic tool in patients
suspected of having prerenal AKI. Renal causes of oliguria are in rare instances diagnosed
by renal biopsy.
IV. DIAGNOSIS. Early recognition of oliguria and, more importantly, anuria is critical because
it affords the clinician an opportunity to diagnose AKI at an earlier stage, thereby facilitating
prompt treatment and prevention of permanent renal dysfunction (9). Hospitalization is usu-
ally necessary to treat the life-threatening complications of AKI. A thorough history and physi-
cal exam, evaluation of the serum blood urea nitrogen to creatinine ratio, the urine sediment,
FENa, and renal ultrasound often lead to an accurate diagnosis.
REFERENCES
1. Klahr S, Miller SB. Acute oliguria. N Engl J Med 1998;338:671–675.
2.
Behrman RE, Kliegman RM, eds. Nelson essentials of pediatrics, 4th ed. Philadelphia, PA: WB Saunders,
2002.
3. Feest TG, Round A, Hamad S. Incidence of severe acute renal failure in adults: results of a community
based study. BMJ 1993;306:481–483.
4. Elasy TA, Anderson RJ. Changing demography of acute renal failure. Semin Dial 1996;9:438–443.
5. Khalil P, Murthy P, Palevsky PM. The patient with acute kidney injury. Prim Care Clin Office Pract
2008;35:239–264.
6. Klahr S. Pathophysiology of obstructive nephropathy. Kidney Int 1983;23:414–426.
7.
Rose BD. Pathophysiology of renal disease, 2nd ed. New York, NY: McGraw-Hill, 1987.
8. Carvounis CP, Nisar S, Guro-Razuman S. Significance of the fractional excretion of urea in the dif-
ferential diagnosis of acute renal failure. Kidney Int 2002;62:2223–2229.
9. Macedo E, Malhotra R, Bouchard J, Wynn SK, Mehta RL. Oliguria is an early predictor of higher
mortality in critically ill patients. Kidney Int 2011;80:760–767.
Table 10.6.2 Initial Laboratory Testing for Oliguria
Prerenal Renal Postrenal
Serum BUN:creatinine
>20:1 <20:1 >20:1
Fractional excretion sodium (%)
<1 >1
Variable
Urine sodium (mmol/L)
<20 >40 >20
Fractional excretion urea (%)
<35 <60
BUN, blood urea nitrogen.
231
10.7
I. BACKGROUND. Priapism is defined as a persistent, often painful, penile erection not
associated with sexual stimulation. No time course is specifically defined, but priapism is
usually diagnosed when the erection lasts greater than 4 hours. Although relatively uncom-
mon (incidence 1.5 per 100,000 person-years and 2.9 per 100,000 person-years for men aged
40 years and older) (1), priapism often represents a urologic emergency (2).
II. PATHOPHYSIOLOGY
A. Etiology.
Two types of priapism (low flow or veno-occlusive and high flow or arterial) have
been described based on the underlying precipitating event (3). Arterial priapism usually
occurs after injury to the cavernous artery from perineal or direct penile trauma. This injury
then leads to uncontrolled high arterial inflow within the corpora cavernosa. Veno-occlusive
priapism is characterized by inadequate outflow and is far and away the most common.
Distinction between the two is imperative since ultimate treatment varies significantly.
B. Epidemiology. A history of penile or perineal trauma almost always precedes arterial
priapism and is the most important historic information that distinguishes between the two
types of priapism. The injury may be related to direct trauma to the penis or pelvic region
(2) or with less severe trauma such as with penile body piercing (4) or penile tattooing (5).
Studies have suggested that up to 41% of patients who present with priapism (veno-occlu-
sive) have taken some type of psychotropic medication, usually neuroleptics, trazodone,
and alpha-blockers such as prazosin (6). Priapism has been commonly reported (1–17%)
after intracavernous injection with prostaglandins for the treatment of erectile dysfunction.
Other drug- or substance-induced causes include the phosphodiesterase-5 inhibitors such
as sildenafil citrate, testosterone, heparin, warfarin, cocaine, tacrolimus, and even scorpion
toxin (3). Patients with any history of malignancy, especially genitourinary or pelvic carci-
noma and new-onset priapism, should be evaluated for penile metastasis. In a recent review,
20–50% of cases with penile metastases initially presented with priapism (7).
The most common cause of priapism in children is sickle cell disease. It has been
reported that over 60% of all sickle cell disease children eventually develop priapism (8).
III. EVALUATION
A. History and Physical.
Specific questions may help identify the type of priapism, cause,
and urgency of treatment. Always inquire how long the priapism has been present. Have
they had “stuttering” symptoms (priapism lasting less than 4 hours that resolves spontane-
ously but then recurs)? How much pain does the patient experience? Moderate to severe,
persistent pain is characteristic of veno-occlusive priapism and results from tissue ischemia.
Pain is generally much more mild or transient with arterial priapism. Is there a history of
penile or perineal trauma? Trauma more commonly precedes arterial priapism. Does the
patient take any medications that may predispose to priapism? Is there any history of malig-
nancy? Is there any history of sickle cell disease or any other vaso-occlusive disease?
The physical should include a thorough genitourinary exam to look for trauma or
malignancy. The corpora cavernosa but not the corpora spongiosum is involved with pria-
pism, and therefore, the glans will remain flaccid while the shaft is erect and tender. The
examination should also include palpation for inguinal lymphadenopathy (genitourinary
(GU) malignancy) and an abdominal exam (abdominal or GU malignancy and trauma).
B. Laboratory Tests. In most instances, the history and physical exam will determine the
cause of priapism. A complete blood count and sickle cell screen may be useful, looking
for malignancy and sickle cell disease, respectively. Coagulation studies are also recom-
mended (in case aspiration is contemplated for treatment). Blood gas measurement from a
P
riapism
David B. Feller
232
cavernosal sample may be useful if differentiation between low- and high-flow priapism is
difficult (2).
In most cases, further diagnostic testing is not needed. If objective studies are needed,
color duplex ultrasonography is the method of choice followed by penile scintigraphy and
magnetic resonance imaging. If pelvic malignancy is suspected, computed tomography is
generally the next step. If trauma preceded priapism, arteriography may be indicated.
C. Genetics. Sickle cell anemia, an autosomal recessive disorder, is associated with a high
incidence of priapism (over 40% of adults and over 60% of children).
IV. DIAGNOSIS
A. Differential Diagnosis.
The key to determining the cause of priapism is the clinical his-
tory. Examination will reveal an erect, usually tender penis with flaccid glans. Early distinction
between arterial and veno-occlusive priapism should be done, with the former often associated
with trauma and less painful or painless erections. If the penis is only partially erect, ischemic
priapism is less likely. Evaluation of priapism is aimed at determining how long it has been
present, since permanent damage may occur within as little as 4 hours, and at determining the
cause. The most common causes are due to psychotropic medications or medications for erec-
tile dysfunction. Less common causes include trauma, sickle cell disease, and pelvic malignancy.
B. Clinical Manifestations. Priapism is considered a urologic emergency and should be man-
aged aggressively. Without prompt recognition and treatment, priapism may result in urinary
retention, cavernosa fibrosis, impotence, or even gangrene. Treatment within 4–6 hours of onset
has been shown to decrease morbidity, the need for invasive procedures, and impotence (6).
REFERENCES
1. Eland IA, van der Lei J, Strickler BH, Sturkenboom MJ. Incidence of priapism in the general popula-
tion. Urology 2001;57:970–972.
2. Burnett AL, Bivalacqua TJ. Priapism: new concepts in medical and surgical management. Urol Clin
North Am 2011;38:185–194.
3. Huang YC, Harraz AM, Shindel AW. Evaluation and management of priapism: 2009 update. Nat Rev
Urol 2009;6:262–271.
4. Holbrook, J, Minocha J, Laumann A. Body piercing: complications and prevention of health risks. Am
J Clin Dermatol 2012;13(1):1–17.
5. Zargooshi J, Rahmanian E, Motaee H, et al. Nonischemic priapism following penile tattooing. J Sex
Med 2012;9(3):844–848.
6. Thompson JW Jr, Ware MR, Blashfield RK. Psychotropic medication and priapism: a comprehensive
review. J Clin Psych 1990;51:430–433.
7. Lin, Yu-H, Kim J, Stein N, et al. Malignant priapism secondary to metastatic prostatic cancer: a case
report and review of the literature. Rev Urol 2011;13(2):90–94.
8. Morrison BF, Burnett AL. Priapism in hematological and coagulative disorders: an update. Urology
2011;8:223–230.
10.8
I. BACKGROUND. The term scrotal mass is general and includes discrete masses such as carcino-
mas as well as general swelling. Scrotal masses can be benign, anatomic, infectious, or malignant
in origin. The clinical significance can range from entirely benign to emergent requiring imme-
diate surgical treatment. The differential diagnosis of scrotal masses can be classified on the
basis of anatomy: skin, spermatic cord, epididymis, and testis. Skin lesions include sebaceous
cysts, cellulitis to include Fournier’s disease (necrotizing fasciitis of the perineum and scrotum),
and squamous cell carcinoma. Lesions of the spermatic cord include indirect inguinal hernia,
Scrotal Mass
Ernestine M. Lee and Eddie Needham
233
varicocele, hematocele, torsion of the appendix testis, and hydrocele. Epididymal swelling
could represent epididymitis or spermatocele. Testicular masses include hydrocele, carcinomas,
varicocele, testicular torsion, and orchitis (1).
II. PATHOPHYSIOLOGY. During the evaluation of any scrotal mass, the primary goal is to deter-
mine whether immediate referral is indicated, as in the case of testicular torsion, Fournier’s
disease, and hernias that are incarcerated or strangulated (2). Torsion is a surgical emergency.
Testicular salvage is 90% when detorsion is performed within 6 hours of symptom onset (1).
III. EVALUATION
A. History
1. Trauma. Only 10% of patients presenting with testicular torsion report antecedent
trauma (1). Hematoceles are more frequently associated with direct trauma (2).
2. Pain. Acute pain (<24 h) is more likely to be associated with torsion, orchitis, epididy-
mitis, hematocele, incarcerated or strangulated hernias, or Fournier’s disease (1–3). More
indolent pain is associated with non-incarcerated or strangulated hernias, hydroceles,
skin infection depending on cause, and tumors. In some cases, masses are painless as is
the case with some tumors, varicoceles, and some hydroceles (2).
3. Patient Age. Scrotal masses of a variety of pathology can occur throughout the life
span. Varicoceles occur in 15% of the male population (3). The most common cause of
acute mass in children up to age 13 years is torsion of the appendix testis (4). Testicular
tumors are the most common malignant tumors encountered in men aged 25 to 35
years (1).
4. Gastrointestinal Symptoms. Patients with torsion, epididymo-orchitis, and some cases
of epididymitis may also complain of nausea. Emesis may be present with torsion (1).
5. Symptoms of Infection. Fever can accompany cellulitis, Fournier’s disease, epididymi-
tis, and orchitis. Patients with Fournier’s disease will often exhibit signs of systemic infec-
tion such as hypotension, vomiting, and lethargy (1, 2). A history of penile discharge
is often found in patients with epididymitis. In up to 80% of patients with mumps,
orchitis symptoms are first observed within 8 days of involvement of the salivary gland
(5). Tuberculosis and syphilis can also cause orchitis.
6. Sexual History. Risk factors for sexually transmitted illnesses increase the possibility of
epididymitis. Traumatic intercourse may lead to hematocele.
7. Other Symptoms. Weight loss, poor appetite, night sweats, and fever may herald meta-
static cancer. A mass that changes size may suggest communicating hydrocele.
B. Physical Examination
1. Exam Position. The standing position may accentuate a varicocele or hydrocele, espe-
cially if accompanied by the Valsalva maneuver. Prehn’s sign, in which gentle elevation
of the affected testicle relieves pain, suggests epididymitis.
2. Palpation. The testes are slightly oblong in shape. Asking the patient to demonstrate
the mass can be quite beneficial. A varicocele, most frequently located on the left, feels
like a cord of worms and lies between the testicle and the inguinal canal. A spermatocele
lies as a firm nodule in the spermatic cord. A hydrocele can be a diffuse unilateral scrotal
enlargement. Testicular torsion is quite painful to palpation.
3. Neurologic Exam. The cremasteric reflex is performed by gently stroking the medial
thigh. Normally, the ipsilateral testicle will rise perhaps 5–10 mm toward the inguinal
canal. With testicular torsion, the cremasteric reflex may be absent.
4. Transillumination. Holding a light against the skin of the scrotum will demonstrate
transillumination with a hydrocele. The scrotal sac will appear red as the light diffuses
through the fluid.
5. General Exam. The left testicle tends to rest slightly lower and more posterior in most
men. The epididymis is generally located on the superomedial pole. The testicular
appendix is not palpable in most men but can become painful, enlarged, and dark with
torsion and strangulation (Blue dot sign). With metastatic disease, regional and general-
ized lymphadenopathy may be present.
234
C. Testing
1. Imaging. For suspected acute torsion, Doppler ultrasound is frequently the easiest and
most readily available modality. The waveforms will demonstrate decreased or absent
blood flow to the affected testis. Sensitivity for torsion is 86–88% and specificity is
90–100. Urology consultation should be considered at the time of ordering Doppler
ultrasound so as not to delay surgical treatment and preserve the testis.
2. Laboratories. If testicular cancer is suspected, consider tumor markers: human chorionic
gonadotropin, AFP (alfa-fetoprotein).
IV. DIAGNOSIS. Testicular torsion is the most emergent scrotal mass. The diagnosis is usually
straightforward given the level of pain and the acuity. Incarcerated hernias may likewise have
an urgent presentation. The non-testicular inguinal mass suggests this diagnosis. Many benign
scrotal masses present over weeks to months and can be diagnosed with the history, physical
exam, and ultrasound. Infectious causes of scrotal masses have a subacute course.
REFERENCES
1. Tiemstra JD, Kapoor S. Evaluation of scrotal masses. Am Fam Physician 2008;78:1165–1170.
2. Davis JE, Silverman M. Scrotal emergencies. Emerg Med Clin North Am 2011;29:469–484.
3. Montgomery JS, Bloom DA. The diagnosis and management of scrotal masses. Med Clin North Am
2011:95;235–244.
4. Lewis AG, Bukowski TP, Jarvis PD. Evaluation of acute scrotum in the emergency department.
J Pediatr Surg 1995;6:637–646.
5. Beard CM, Benson RC Jr, Kelalis PP, Elveback LR, Kurland LT. The incidence and outcome of
mumps orchitis in Rochester, Minnesota, 1935 to 1974. Mayo Clin Proc 1977;52:3–7.
10.9
I. BACKGROUND
A. Definition.
Scrotal pain can be acute, intermittent, or chronic. Chronic scrotal pain is pain last-
ing over 3 months. Scrotal pain is a common problem in adults and the incidence is unknown.
Scrotal pain can result from pathology within the scrotum, trauma to the scrotum, scrotal sac,
or extra-scrotal pathology, referred pain from intra-abdominal pathology, or systemic diseases.
Scrotal and testicular problems may range from benign to malignant and debilitating conditions.
Most common causes of scrotal pain are due to benign conditions like epididymitis, varicocele
(postvasectomy is a common reason) (1), hydrocele, spermatocele, polyarteritis nodosa, and
epididymal or testicular cysts. With the exception of trauma or torsion of testis, scrotal pain in
an adult rarely requires emergent surgical intervention. Testicular torsion is common in child and
adolescent population (1 in 4,000 males younger than 25 years) and requires urgent intervention
(2). The risk of testicular torsion includes malformations, increase in testicular volume, testicular
tumor, testicles with horizontal lie, a history of cryptorchidism, and a long spermatic cord.
Trauma is a less common cause of torsion. The testis may be salvaged if appropriately treated in
time (90% < 6 hours and 50% in 12 hours and <10% at 24 hours) (3).
II. PATHOPHYSIOLOGY
A. Etiology
1. Intrascrotal Pathology. Testicular torsion (torsion of testicular appendage), spermatic
cord torsion (intravaginal, extravaginal, acute, or intermittent), epididymitis, orchitis,
vasculitis (e.g., Henoch-Schönlein purpura), varicocele, spermatocele, and primary or
metastatic testicular tumor.
Scrotal
P
ain
George P. Samraj
235
2. Pathology of the Scrotal Sac. Infections, early Fournier gangrene, trauma, animal or
insect bites, cysts and idiopathic scrotal edema, and sexual abuse.
3. Extrascrotal Pathology. Direct/indirect hernia, incarcerated hernia, hydrocele (commu-
nicating hydrocele or encysted hydrocele with or without torsion or associated with acute
abdominal pathology, e.g., appendicitis, peritonitis, splenic rupture), associated urinary
tract infection (UTI), prostatitis, and sexually transmitted disease (STD).
4. Pain Referred from Intra-abdominal Pathology or Systemic Disease. renal colic,
mononucleosis, Coxsackie B virus, Buerger’s disease, and polyarteritis nodosa.
B. Epidemiology
1. Intrascrotal Pathology
a. Testicular torsion: Torsion can occur at any age, but is uncommon in adults. In
pediatric patients, appendix testis torsion is more common (40–60%) than spermatic
cord torsion (20–30%) (4). Peak age of testicular torsion is 12–16 years and most
(86–93%) occur after age 10 years. Intrascrotal pathology is the most common cause
of scrotal pain in the first year of life (often misdiagnosed as colic or intra-abdominal
disorder).
b. Epididymitis: Epididymitis is the most common cause of acute scrotal pain in adults.
Epididymitis in children can be due to infectious or noninfectious causes. If it occurs
in prepuberty, suspect urogenital anomaly or dysfunction.
c. Orchitis: Orchitis is usually due to extension of epididymitis. Approximately 20% of
postpubertal mumps infection produces mumps orchitis. Approximately 70% of cases
are unilateral. This is less common since the mumps vaccine (5).
d. Varicocele: It is an abnormal dilatation of the pampiniform plexus veins due to
increased pressure secondary to the venous backflow associated with incompetent
valves in the spermatic vein. This is common in adults and adolescents. It is uncom-
mon in prepubertal children. Intra-abdominal lesion obstructing venous drainage may
present with acute rupture or thrombosis.
e. Testicular tumor: This can be primary or secondary. Testicular cancer accounts for 1% of
all male cancers, and it is the leading cause of cancer among men aged between 15 and
35 years. Most cancers are germ cell in origin and few (4%) are sex cord-stromal tumors.
f. Spermatocele (epididymal cyst): This is a benign cystic collection of fluid which arises
from the epididymis, common after vasectomy, not seen in prepuberty, and very rare
in adolescents.
2. Extrascrotal Pathology
a. Direct/indirect hernia, incarcerated hernia. This is equally prevalent in adults and
children.
b. Hydrocele: Primarily in neonates. Often resolves spontaneously in the first year. If
it persists beyond the second year, surgical consultation may be required. Occurs in
adults, but not common.
c. Prostatitis/UTI/STD. UTI should be considered in young children. If the patient has
UTI, further evaluation of urinary tract for reflux or congenital anomalies needs to
be done. If STD is diagnosed, sexual abuse should be considered in children. STD is
common in adolescents and adults.
C. Scrotal Trauma
1. Significant damage to a testicle from trauma, in any age group, is rare. Scrotal trauma
with straddle injury, bicycle handle bars injury, and sports injury is common. Scrotal
pain due to trauma is generally self-evident or self-reported. Traumatic damage in pre-
puberty is rare due to small testicles. Testicular pain lasting more than an hour after a
traumatic injury is evaluated for testicular rupture or hematoma.
III. EVALUATION
A. History
1. A comprehensive history is essential for the evaluation of scrotal pain. The patient’s
age, onset, severity of the pain, and sexual history are essential for diagnosis. The speed
of worsening symptoms and signs, associated symptoms like fever, nausea, vomiting,
urinary symptoms, and history of urethral discharge are noted. Conditions affecting the
236
scrotum may be secondary to abdominal pathology. Epididymitis usually occurs in one
testis and progressively gets worse over days to weeks, whereas testicular torsion is sudden
and abrupt in onset. Histories of previous episodes were noted in many patients with
torsion. Time of onset of symptoms of torsion is immensely useful in managing torsion
and the outcome.
2. History of trauma needs to be elicited. Torsion of testicular appendage has less intense
pain than testicular torsion. Epididymitis can be abrupt or insidious in onset. Fever and
voiding symptoms may be present with epididymitis.
B. Physical
1. A comprehensive physical examination is essential for the diagnosis of scrotal diseases. A
focused exam should include observation and examination of the abdomen, scrotum, geni-
tal organs, and prostate when indicated. Typical examination includes inspection, palpa-
tion, and transillumination of the scrotum when indicated. Scrotum is noted for swelling,
color change, ulcers, or evidence of trauma or asymmetry. In small children, observation
for irritability, restlessness, and crying is helpful in diagnosing severe conditions. Any
neonate or small child with abdominal pain should be observed for scrotal conditions.
Testicular numbers and locations should be noted to rule out cryptorchidism. The scrotum
is examined for evidence of trauma, unilateral or bilateral swelling, infection, or masses.
Discoloration is usually due to trauma, but can be seen with torsion and epididymitis. The
cremasteric reflex is the most sensitive physical finding for testicular torsion. The specificity
of this test varies with age group. If cremasteric reflex is present on the painful side, testicu-
lar torsion may be ruled out in most cases. In order for the absence of a cremasteric reflex
to be a reliable indicator, its presence must be demonstrated on the nonpainful side. Other
useful findings of torsion include Prehn’s sign (elevation of testis increases pain for torsion
and reduced pain in epididymitis), elevation of scrotum on the affected side, abnormal
testicular lie, and abnormal and exquisitely tender testis. Unilateral swelling without skin
changes indicates hernia or hydrocele. Palpation of the scrotum is performed for the assess-
ment of edema, infections, or other skin conditions. Transillumination of the scrotum may
differentiate a hydrocele from hematocele. Focal tenderness at the upper pole of testis and
“blue dot sign” (necrotic appendix seen through the scrotal skin) may be present in torsion
of appendix. However, this sign is also observed in torsion of the testis (6).
C. Laboratory Tests. Very few laboratory tests are indicated in the evaluation of scrotal pain.
1. Urinalysis (UA): It is performed to rule out bacteriuria or pyuria. Usually positive UA is
helpful in differentiating epididymitis from testicular or appendiceal torsion. However,
pyuria may be present with torsion and may create diagnostic confusion.
2. Complete blood count (CBC) and comprehensive metabolic panel (CMP): Leukocytosis is
a nonspecific finding. More commonly, it is elevated in epididymitis and in late stages (after
24 hours) of testicular or appendiceal torsion. Occasionally, a CMP may be beneficial in
identifying the causes of scrotal swelling (e.g., hypoproteinemia or liver or kidney failure).
D. Imaging
1. Color Doppler ultrasound examination (CDUS): CDUS is the first-line modality for
the diagnosis of torsion after history and physical. CDUS provides a definitive diagnosis
of testicular torsion in 91.7% of cases. However, it is less reliable (63–90% sensitive)
in spermatic cord torsion. The findings of torsion in CDUS include reduced or absent
Doppler waveforms, parenchymal heterogeneity, and/or altered echotexture compared
with the contralateral testis. High-resolution ultrasonography may improve the diagnos-
tic accuracy when available.
2. Nuclear Scan: It measures testicular perfusion with high sensitivity and specificity in tes-
ticular torsion. However, the process is often too slow to be used universally in determin-
ing the need for surgical intervention in a narrow therapeutic window. Primary uses are
evaluation in trauma, with asymptomatic masses, and when elective surgical exploration
is contraindicated and Doppler studies are equivocal.
3. Magnetic Resonance Imaging (MRI): MRI provides good anatomic data, but it is not
useful in the acute setting to evaluate for blood flow. It is highly valuable in assessing
cryptorchidism or abdominal pathology contributing to scrotal pain.
237