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on color Doppler is consistent with torsion, and immediate surgical exploration
should be done. There is typically a 4- to 6-hour window before significant ischemic damage occurs. During surgery, detorsion of the affected spermatic cord is
performed until no twists are visible, and testicular viability is then assessed. If still
viable, orchiopexy is performed, in which the testicle is permanently fixed within
the scrotum.
Acute Epididymitis or Epididymo-orchitis
Pathophysiology. Acute epididymitis or acute epididymo-orchitis is the most common cause of scrotal pain in adults. It is caused by inflammation of the epididymis,
which carries sperm from the seminiferous tubules to the vas deferens. Inflammation can frequently spread to the testicle, causing epididymo-orchitis. The most
probable cause of inflammation differs based on the age of the patient. In patients
aged 14 to 35 years old, Neisseria gonorrhoeae or Chlamydia trachomatis infection is
most probable. In patients < 14 years old or ≥ 35 years old, common urinary tract
pathogens, including Escherichia coli, are most likely.
Clinical Presentation. Diagnosis is made primarily by history and physical examination, as well as by ruling out other cases requiring urgent intervention (eg, testicular torsion). Patients commonly present with gradual increasing pain that can
radiate to the lower abdomen. Patients also often have symptoms of a lower UTI
(eg, urgency, frequency, dysuria). On physical examination, patients have localized
pain to the posterior aspect of the testicle that can progress to swelling and tenderness. Patients have a normal cremasteric reflex and also have a positive Prehn
sign (pain relief with testicular elevation). In all suspected cases of epididymitis,
urinalysis, urine culture, and testing for N. gonorrhoeae and C. trachomatis should
be performed. If findings are less clear, scrotal ultrasound should be performed to
confirm the diagnosis, which commonly demonstrates an enlarged/thickened epididymis with increased blood flow on color Doppler.
Treatment. Treatment usually involves oral antibiotics, nonsteroidal antiinflammatory drugs (NSAIDs), local application of ice, and scrotal elevation. Oral
antibiotic choice is also stratified based on age/risk factors. In patients who are
under 35 or who are at risk for sexually transmitted infections (STIs), ceftriaxone
(250 mg IM for one dose) plus doxycycline (100 mg orally twice daily for 10 days)
is recommended. For patients ≥ 35 years of age and with low risk of STI, recommended treatment is levofloxacin (500 mg orally once daily for 10 days).
Prostatitis
Prostatitis can be due to inflammation or infection of the prostate and can be acute
or chronic in nature. Infection is commonly due to coliform bacteria, followed by
N. gonorrhoeae and C. trachomatis. Affected patients present with dysuria, pain on
ejaculation, and dull pain in less severe cases, while in acute cases patients may be
febrile and have malaise. Diagnosis is often clinical and should include a digital
rectal examination, which often reveals a boggy and tender prostate. Urinalysis may
show leukocyte esterase and/or nitrates when infection contaminates the urine,
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and a urine culture should be obtained. Rarely, prostate massage for examination
and culture of seminal fluid may aid in diagnosis. Treatment of acute and suspected
infectious cases includes a 4-week course of trimethoprim-sulfamethoxazole, doxycycline, or ciprofloxacin and NSAIDs. Cases thought to be noninfectious generally
improve with NSAIDs alone.
Erectile Dysfunction
Pathophysiology. ED is a common occurrence in men, with a prevalence that
increases with age. There are numerous causes for this, including vascular, psychological, neurologic, and hormonal factors. Rapid clinical assessment of ED
can be performed with the five-question International Index of Erectile Function
(IIEF-5), which includes questions about confidence, ability to penetrate, maintenance of erection, ability to ejaculate, and satisfaction. Further clarification of
the etiology of ED is based on history and physical examination, including genital
examination and assessment of secondary sex characteristics.
History taking can help to differentiate psychogenic causes from organic medical causes. Young age, preserved nocturnal erections, and partner conflict support
ED of psychogenic nature. A nocturnal penile tumescence test, an overnight test to
check for sleep erection, can help clarify this. Men with ED should be evaluated for
potential underlying cardiovascular disease due to the common pathophysiologic
etiology of endothelial dysfunction. Laboratory evaluation of patients with ED
should include fasting glucose or hemoglobin A1c testing, lipid panel, and morning
testosterone evaluation.
Treatment. Treatment includes optimizing the management of concomitant
medical diagnoses, such as diabetes mellitus, hyperlipidemia, hypogonadism, and
metabolic syndrome, while eliminating tobacco and minimizing alcohol. Medications that may contribute to ED include beta-blockers, calcium channel blockers,
antidepressants, antihistamines, antipsychotics, and some diuretics. First-line therapy includes lifestyle modifications, medication changes, and oral phosphodiesterase type 5 inhibitors (PDE-5 inhibitors; eg, sildenafil). Other therapies include
injectable or intraurethral alprostadil, vacuum pump erection devices, or surgically
implantable penile prostheses. Testosterone replacement therapy may improve
erectile function in some patients. PDE-5 inhibitors are contraindicated in patients
taking nitrates, as life-threatening hypotension can occur.
CASE CORRELATION
See also Case 14 (Hematuria) and Case 45 (HIV, AIDS, and Other Sexually
Transmitted Infections).
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COMPREHENSION QUESTIONS
16.1 A 60-year-old man reports increased urinary frequency and has been having
decreased flow of his urinary stream. He has a history of hypertension controlled with hydrochlorothiazide but has been otherwise healthy. He reports
that his father had a similar issue in his 70s. Rectal examination reveals a
grossly enlarged prostate without any tenderness, nodules, or asymmetry.
Which of the following is a reasonable initial therapy for treatment of this
patient’s symptoms?
A. Referral for prostatectomy
B. Terazosin 1 mg at bedtime
C. Oxybutynin 5 mg twice daily
D. Empiric antibiotic therapy for presumed infection
16.2 A 21-year-old man reports scrotal pain over the past 4 days. The pain has
been radiating to his lower abdomen. He has been sexually active for a few
weeks with a new female partner. On physical examination, he has a normal
cremasteric reflex and has some relief of pain upon elevation of the scrotum.
What is an appropriate choice for empiric antibiotics?
A. Azithromycin 1 g orally one time
B. Ceftiraxone 250 mg IM one time and doxycycline 100 mg orally twice
daily for 10 days
C. Levofloxacin 500 mg orally daily for 10 days
D. Ofloxacin 300 mg orally twice daily for 10 days
16.3 A 27-year-old man reports issues obtaining erections during sexual intercourse. He has no significant past medical history. He reports obtaining
erections at nighttime. His general physical examination and GU exam are
normal. What is the most appropriate initial step in management?
A. Start on sildenafil 50 mg 1 hour before sexual activity as needed
B. Prescribe sublingual nitroglycerin
C. Ask about his relationship and potential stressors
D. Prescribe supplemental intramuscular testosterone 75 to 100 mg/week
ANSWERS
16.1 B. This patient most likely has BPH—he is an older man with increased
frequency, difficulty voiding, and a symmetrically enlarged prostate without
nodularity on examination. Initial therapy often involves lifestyle modification, such as fluid restriction at night, and the use of an oral alpha-blocker,
such as terazosin. This agent also has the benefit of treating the hypertension. Answer A (referral for prostatectomy) is indicated for acute urinary
retention, persistent or recurrent urinary infections, recurrent hematuria, and renal insufficiency due to chronic bladder outlet obstruction.
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Thepatient does not have any of these findings. Answer C (oxybutynin)
can help with some of the symptoms of frequency but does not decrease
the size of the prostate or affect blood pressure. Answer D (empiric antibiotics) is not indicated since the patient has no symptoms of infection, such as
dysuria, urgency, or fever.
16.2 B. This patient most likely has epididymitis. In his age group and with the
history of a new sexual partner, gonorrhea or chlamydia is the most likely
causes. The most appropriate antibiotic is a combination of ceftriaxone and
doxycycline to cover both bacteria. Azithromycin (answer A) is a good alternative if the patient cannot tolerate doxycycline; however, this would not
cover N. gonorrhea. Levofloxacin (answer C) and ofloxacin (answer D) are
both reasonable options if the patient were ≥ 35 years old and not at high risk
for an STI.
16.3 C. This patient is presenting with ED. It is important to understand what the
etiology might be. He is young and healthy and has preserved nighttime erections, which are all factors that favor psychogenic ED. The next step would be
to probe about relationship issues and other stressors. Sildenafil (answer A)
is a first-line drug for ED that is due to an organic medical cause (ie, coronary
artery disease). Nitrates (answer B) are drugs commonly prescribed for angina
and are contraindicated when on PDE-5 inhibitors like sildenafil. Testosterone (answer D) would only have some efficacy if the patient had a proven low
testosterone level.
CLINICAL PEARLS
» BPH is the most common cause of LUTS in older men. Its management is
completely based on symptoms.
» If testicular torsion is likely, do not waste time with ultrasound; surgical
exploration is imperative.
» Patients with epididymitis demonstrate a positive Prehn sign and have a
cremasteric reflex, which are both absent in testicular torsion.
» Psychogenic ED usually can be distinguished from ED of organic medical
causes by a patient history of preserved nocturnal erections.
REFERENCES
Dahm P, Brasure M, MacDonald R, et al. Comparative effectiveness of newer medications for lower
urinary tract symptoms attributed to benign prostatic hyperplasia: a systematic review and meta-
analysis. Eur Urol. 2017;71:570-581.
McConaghy JR, Panchal B. Epididymitis: an overview. Am Fam Physician. 2016;94(9):723-726.
McVary KT, Roehrborn CG, Avins AL, et al. Association guideline: management of benign prostatic
hyperplasia. American Urological Association; 2010. https://www.auanet.org/documents/education/
clinical-guidance/Benign-Prostatic-Hyperplasia.pdf. Accessed May 27, 2019.
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Platz EA, Joshu CE, Mondul AM, et al. Incidence and progression of lower urinary tract symptoms in a
large prospective cohort of United States men. J Urol. 2012;188:496-501.
Rew KT, Heidelbaugh JJ. Erectile dysfunction. Am Fam Physician. 2016;94(10):820-827.
Scher HI, Eastham JA. Benign and malignant diseases of the prostate. In: Jameson J, Fauci AS,
Kasper DL, Hauser SL, Longo DL, Loscalzo J, eds. Harrison’s Principles of Internal Medicine.
20th ed. New York, NY: McGraw Hill; 2018: Chap. 83. http://accessmedicine.mhmedical.com/
content.aspx?bookid=2129§ionid=192016319. Accessed May 27, 2019.
Serlin DC, Heidelbaugh JJ, Stoffel, JT. Urinary retention in adults: evaluation and initial management.
Am Fam Physician. 2018;98(8):496-503.
Sharp VJ, Kieran K, Arlen AM. Testicular torsion: diagnosis, evaluation, and management. Am Fam
Physician. 2013;88(12):835-840.
Trojian, TH, Lishnak TS, Heiman D. Epididymitis and orchitis: an overview. Am Fam Physician.
2009;79(7):583-587.
CASE 17
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A 58-year-old woman presents to your office for follow-up of an emergency
department visit. She was seen 1 week earlier in the emergency department
for abdominal pain and was diagnosed with nephrolithiasis. Ultimately, she
was sent home with pain medications and given instructions to strain her
urine for stones and to follow up with her primary care provider. Today, she
is asymptomatic. She takes no medications on a regular basis. Her family
history is significant only for a father with high blood pressure. She had several
routine laboratory tests drawn in the emergency department, copies of which
she brings with her. Upon your review of the laboratory values, you note the
following (normal values are in parentheses): sodium 142 mEq/L (135-145);
potassium 4.0 mEq/L (3.5-5.0); chloride 104 mg/dL (95-105); bicarbonate
28 mEq/L (20-29); blood urea nitrogen (BUN) 20 mg/dL (7-20); creatinine
0.9 mg/dL (0.8-1.4); calcium 12.5 mg/dL (8.5-10.2); and albumin 4.2 g/dL
(3.4-5.4). The complete blood count (CBC) was within normal limits.
The renal calculus was detected by helical computed tomographic (CT)
scanning without contrast and was located in the right midureter. Your patient
has brought with her the stone that she has strained from the urine. Upon
questioning, you learn that she has had multiple episodes of “kidney stones” in
the past 2 years. You send the stone to the laboratory for analysis and order a
repeat serum calcium level. The results show that the stone is made of calcium
oxalate, and the patient’s serum calcium is still elevated at 11.9 mg/dL.
▶ What is the most likely diagnosis?
▶ What is the most likely cause?
▶ What is the next step?
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ANSWERS TO CASE 17:
Electrolyte Disorders
Summary: This 58-year-old woman presents with
A history of recurrent nephrolithiasis, presenting for follow-up
Calcium oxalate stones
An initial serum calcium level that was elevated, as was the repeat serum calcium
1 week later
Asymptomatic presentation
No medications and a family history only significant for hypertension
Most likely diagnosis: Hypercalcemia and recurrent nephrolithiasis.
Most likely cause: Hyperparathyroidism.
Next step: Further laboratory workup, including serum parathyroid hormone
(PTH) level.
ANALYSIS
Objectives
1. Be able to list common causes of calcium, sodium, and potassium disorders.
(EPA 1, 2)
2. Describe the workup and management of common electrolyte disorders.
(EPA 4, 10)
Considerations
This patient illustrates one common presentation of hypercalcemia. Many times,
patients with hypercalcemia are asymptomatic, and an elevated calcium level is
found unexpectedly on routine laboratory studies. The diagnostic workup begins
with a careful review of the patient’s history, as clues to its etiology may often be
elicited here. The diagnostic workup is designed to distinguish parathyroid dysfunction from other etiologies so that optimal treatment and management can be
pursued.
APPROACH TO:
Electrolyte Disorders
DEFINITIONS
HYPERPARATHYROIDISM: Condition of elevated PTH usually due to excessive production by the parathyroid glands, leading to hypercalcemia.
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SECONDARY HYPERPARATHYROIDISM: Condition that occurs as the
parathyroid glands overproduce PTH to respond to low serum calcium levels. This
may occur as a response to low dietary calcium intake or a deficiency of vitamin D.
TERTIARY HYPERPARATHYROIDISM: Elevated PTH in patients who have
renal failure.
CLINICAL APPROACH TO HYPERCALCEMIA
Calcium Homeostasis
Before discussing the differential diagnosis of hypercalcemia, it is essential to
review the basic mechanism by which normal calcium levels are maintained in the
body. Most of the calcium in the body is found in the skeleton (approximately 98%).
The remaining calcium is found in circulation. Of this remaining 2%, about half
is bound to albumin and other proteins, and half is “free,” or ionized. It is the ionized calcium that has physiologic effects. Because the serum calcium is partially
bound to albumin, abnormally low serum albumin levels will affect the measurement of calcium, thus causing a misinterpretation of an abnormal calcium level.
With patients found to have a concomitant hypoalbuminemia, the ionized calcium
can be measured directly. However, there is a useful formula that can correct for
this error. A “corrected” serum calcium is provided by the formula
Corrected serum calcium =
[0.8 × (Normal albumin) – (Patient’s albumin level)] + (Serum calcium)
PTH, calcitonin, and 1,25-dihydroxyvitamin D3 (calcitriol) are responsible for
regulating calcium levels and maintaining calcium homeostasis. Causes of hypercal-
cemia include an increase in calcium resorption from bone, a decrease in renal excretion of calcium, or an increase in calcium absorption from the gastrointestinal (GI)
tract. When calcium levels increase, calcitonin, produced by the thyroid parafol-
licular cells, attempts to lower calcium levels through renal excretion of calcium and
by opposing osteoclast activation. When calcium is excreted through this pathway,
phosphate is also excreted. Conversely, low levels of circulating calcium normally
result in PTH secretion. This promotes osteoclast activation, which mobilizes
calcium from bone and affects calcium resorption at the kidneys, thereby retaining circulating calcium. While PTH will increase the calcium in the blood, it has
the opposite effect on serum phosphate levels. PTH also increases calcitriol levels,
which act at the GI tract to promote both calcium and phosphate absorption.
Pathophysiology of Hypercalcemia
Any process that increases GI calcium absorption, decreases renal excretion, or
activates osteoclastic activity will raise serum calcium levels. If this occurs beyond
the normal bounds of maintaining calcium homeostasis, hypercalcemia will occur.
The most common cause of hypercalcemia in the ambulatory patient is hyperparathyroidism. Cancer is the second leading cause. Hyperparathyroidism and cancer
combined account for 90% of hypercalcemia cases. It is useful to categorize the etiologies of hypercalcemia into five main areas: PTH, malignancy, renal failure, high
bone turnover, and those related to vitamin D (Table 17–1).
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Table 17–1 • COMMON CAUSES OF HYPERCALCEMIA
Condition Specific Example Pathophysiology
Increased Bone Resorption
Primary
hyperparathyroidism
Malignancy Solid tumors of lung; squa-
Breast cancer; multiple
Hypervitaminosis A
(vitamin A intoxication)
Immobilization Less common than
Increased Calcium Absorption
Hypervitaminosis D
(vitamin D intoxication)
Granulomatous disease Tuberculosis; sarcoidosis;
Milk-alkali syndrome Excessive intake of calcium-
Miscellaneous
Medications Thiazide diuretics; lithium Reduced urinary excretion of calcium;
Rhabdomyolysis Calcium released from injured muscle
Adrenal insufficiency Increased bone resorption and
Thyrotoxicosis (usually
mild hypercalcemia)
Sporadic or familial; multiple
endocrine neoplasia (MEN)
types 1 and 2
mous carcinoma of head and
neck; renal carcinoma
myeloma; prostate cancer
Includes both vitamin A and its
analogs (used to treat acne)
above causes
Increased calcitriol level leads to
Hodgkin disease
Increased bone resorption
Tumor secretion of PTH-rP
Direct osteolysis
Increased bone resorption
Increased risk when underlying
disorder of high bone turnover
(eg, Paget disease)
increased Gl absorption of calcium
and phosphate
Increase extrarenal conversion of
25-hydroxyvitamin D3 to calcitriol
containing antacids
increased PTH secretion
increased protein binding of calcium
Abbreviation: PTH-rP, parathyroid hormone-related peptide.
History. The first step in the evaluation is a careful history to try to establish a
cause and to assess for manifestations. The history should include family history
of calcium disorders, such as renal stones or malignancy. The patient’s risk factors
for malignancy, such as smoking, should be investigated. The chronicity of symptoms should be taken into account; more acute symptoms suggest malignancy over
hyperparathyroidism and vice versa. A careful review of medications should also
take place, including not only prescription medications but also over-the-counter
supplements. Dietary intake of vitamin D and calcium should be questioned. Furthermore, history of immobilization secondary to a hospital stay or recent injury
should be looked into since prolonged immobilization can cause massive bone
demineralization and hypercalcemia. At this point, if the hypercalcemia is mild and
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EVALUATION OF PATIENTS WITH HYPERCALCEMIA
Hypercalcemia
Key historical considerations
• Confirm if ↑Ca
• Clues from history and physical findings
Acute (or unknown) duration Chronic duration (months)
PTH high PTH highPTH lowPTH low
1˚ Hyperpara thyroidism
Consider MEN
syndromes
Figure 17–1. Algorithm for the evaluation of hypercalcemia. Reproduced with permission, from
Jameson J, Fauci AS, Kasper DL, et al. Harrison’s Principles of Internal Medicine, 20th ed. 2018. Copyright
© McGraw Hill LLC. All rights reserved.
Consider
malignancy
PTHrP assay
Clinical evaluation
Screen
negative
2+
chronic
Other causes
Granulomatous
disease
FHH
Milk-alkali syndrome
Medications
(lithium, thiazides)
Immobilization
Vit D or Vit A
intoxication
Adrenal insufficiency
Hyperthyroidism
Hyperpara thyroidism
Consider MEN
syndromes
the patient asymptomatic, it is acceptable to stop any suspect medication(s) and
repeat the serum calcium level. An algorithm for the assessment of hypercalcemia
is shown in Figure 17–1.
Parathyroid Hormone Levels. If a causative medication is not found, a serum
intact PTH level should be measured. This level will be suppressed, normal, or
elevated. As with many endocrine disorders, it is useful not to think of normal or
abnormal values; rather, one should understand what is appropriate for a given situation. For example, in normal subjects, an increased calcium load will normally
depress the PTH hormone level; thus a low PTH level in this situation is normal,
or appropriately suppressed. If a patient has an elevated calcium level and the PTH
is “normal,” it is said to be inappropriately normal because in the face of hypercalcemia it should be low, or suppressed.
Primary Hyperparathyroidism. If a patient with hypercalcemia has a normal or
elevated PTH level, then the normal feedback loop is not responding. This defines
hyperparathyroidism. Primary hyperparathyroidism occurs when the parathyroid
gland overproduces PTH and does not respond to the negative feedback of elevated calcium levels. The vast majority of primary hyperparathyroidism is caused by
an adenoma (benign tumor) of one of the four parathyroid glands.
Secondary and Tertiary Hyperparathyroidism. Secondary hyperparathyroidism
occurs as the parathyroid glands overproduce PTH to respond to low serum calcium
levels. This may occur as a response to low dietary calcium intake or a deficiency of
vitamin D. Tertiary hyperparathyroidism occurs in patients who have renal failure.
Patients in renal failure initially present with hypocalcemia, hyperphosphatemia,
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