Medscape CME Case Presentations

A 75-Year-Old Man With Anuria and Abdominal Distention CME

Background
Figure 1.

Figure 2.

A 75-year-old man presents to the emergency department (ED) with a 6-week history of worsening
lower abdominal pain. He describes the pain as sharp, constant, and associated with a weight loss
of approximately 20 lb over the past month. The patient states that for the past few weeks he has
also noticed bilateral lower-extremity swelling and abdominal distention. The abdominal distention
has been severe enough to prevent him from bending over. He experienced an increased frequency
of urination until 3 days ago; he has been anuric since then. For the past week he has not been able
to tolerate solid foods, resulting in an entirely liquid diet. As of the day of presentation even
liquids have become intolerable. There is also a history of numbness and tingling in both legs
and an unsteady gait during the last week. He reports a feeling of confusion but is fully oriented to
person, place, and time. His medical history is significant for hypertension under treatment and
mitral valve insufficiency. He denies any surgical history. His current medications include
daily aspirin and nifedipine. The patient has an age-appropriate level of physical activity and lives
alone. He does not smoke or drink.
On physical examination, the patient is a well-oriented elderly man in no acute distress. His
vital signs include an oral temperature of 97.4F (36.3C), a blood pressure of 211/92 mm Hg, a
pulse of
104 beats/min, an unlabored respiratory rate of 20 breaths/min, and an oxygen saturation of 97% on

room air. Head and neck examination reveals dry oral mucous membranes with a supple neck and
no jugular venous distention. The chest examination is clear to auscultation bilaterally, with
normal breath sounds and normal S1 and S2 heart sounds without murmurs, rubs, or gallops. The
abdominal examination is significant for distention, mostly in the hypogastric and umbilical
regions, and for the presence of a reducible umbilical hernia. Normal bowel sounds are appreciated
in all quadrants. The patient's lower abdomen is diffusely tender, with slight tenderness noted in
the upper abdomen as well. There is no rebound tenderness or guarding and Lloyd's sign is
negative. Extremity examination is significant for bilateral pitting edema of the lower extremities.
The patient has no focal neurologic abnormalities (although gait testing is deferred).
Initial laboratory investigations include a complete blood count (CBC) and basic metabolic panel.
There are no significant findings on the CBC. The metabolic panel reveals a serum sodium level
of
130 mEq/L (normal range, 136-145 mEq/L), potassium of 4.2 mEq/L (normal range, 3.5-5.0
mEq/L),
chloride of 83 mEq/L (normal range, 95-105 mEq/L), bicarbonate of 16 mEq/L (normal range, 2228 mEq/L), and glucose of 92 mg/dL (normal range, 70-125 mg/dL). Serum creatinine is 21.2
mg/dL (normal range, 0.6-1.2 mg/dL) and blood urea nitrogen is 120 mg/dL (normal range, 7-18
2
mg/dL). The calculated glomerular filtration rate (GFR) is 3 mL/min/1.73 m (normal, 90
2
mL/min/1.73 m ).
A CT scan of the abdomen and pelvis is obtained (Figures 1 and
2).
What is
diagnosis?

the

most

likely

Hint: Note the decreased GFR in light of the CT findings.

Malignant hypertension
Obstructive uropathy
Renal artery stenosis
Abdominal aortic aneurysm
Renal cell carcinoma

Discussion
The patient's CT scans both with and without contrast revealed moderate bilateral
hydroureteronephrosis without evidence of an obstructing stone in the ureters. The kidneys were
enlarged and perinephric fat stranding was noted (Figure 1). The prostate was also found to be
enlarged and the bladder was noted to be extremely enlarged (Figure 2). A diagnosis of obstructive
uropathy resulting from an enlarged prostate was made.
Total lower urinary tract obstruction (UTO) should be suspected when a patient presents with acute
anuria and other causes, such as a past history of end stage renal disease (ESRD) or shock with
prerenal failure, have been excluded. The most common cause of lower UTO in men is benign
prostatic hyperplasia (BPH).[1] Other possible causes include phimosis, urethral strictures, and
neurogenic bladder. Treatment of prostate cancer by external beam radiation, surgery, and
especially brachytherapy can also result in urinary retention, especially in the initial weeks
following therapy.[2] Anticholinergic medications are a well-known cause of urinary retention.
Diphenhydramine has a similar mechanism and should be administered with caution in the elderly.
Causes of unilateral ureteral obstruction include blood clots, sloughed renal papillae (as can occur
in diabetic nephropathy, analgesic nephropathy, renal tuberculosis, and sickle cell disease), and
renal calculi.[1] Compression of the ureters can be due to neoplasms of adjacent viscera or
aneurysms of the aorta or iliac vessels. Accidental ureteral damage can occur with gynecologic
surgery. Ureteral stasis and compression are common during pregnancy and usually occur on the
right side; however, in rare cases they can present bilaterally. In children, congenital anomalies
such as severe vesicoureteral reflux or posterior urethral valves should be suspected.[3]
The clinical features of complete bilateral UTO include abdominal pain resulting from distention of
the renal (Gerota) fascia or the urinary bladder, difficulty voiding, and hematuria.[4]
Hypertension can result from increased renal secretion of renin.[3] Pain is less pronounced and may
even go unnoticed in cases in which the obstruction progresses gradually. This can result in
patients presenting after irreversible loss of renal function has already occurred. Frequent
urinary tract infections or infections in uncommon populations, such as males and children, should
raise suspicion for a partial or intermittent obstruction. Urine culture in these patients may reveal
atypical organisms (such as Pseudomonas species).
Paradoxically, partial or intermittent UTO may result in polyuria. Extracellular volume expansion
leads to an increased level of atrial natriuretic peptide (ANP), which inhibits sodium reabsorption
at the proximal tubule. Decreased sodium reabsorption diminishes the medullary interstitial
gradient, thereby reducing the concentrating power of the nephron. Further reduction in renal
concentrating power results from a downregulation of the urea transporters responsible for creating
this concentration gradient.[5] A dysfunction of this transporter is also seen in a subset of
congenital diabetes insipidus (DI) patients.[6] Finally, increased ureteral pressure damages the
distal nephron where vasopressin acts to concentrate the urine, creating an acquired nephrogenic
DI.[7] Hypernatremia resulting from obstructive uropathy can be found in sporadic case
reports, but clinicians should be more circumspect of this electrolyte abnormality immediately
following relief of

the obstruction.[8-10] In the above case, the patient was hyponatremic at the time of presentation,
likely from expansion of the effective circulating volume.
UTO can also lead to hyperkalemic renal tubular acidosis (RTA) or type IV RTA. In fact, the
differential diagnosis of hyperkalemic RTA should include an investigation for UTO. This
condition is characterized by hyperkalemia, metabolic acidosis, and impairment of ammonia
excretion (increased urine anion gap). The mechanism of this sequela of UTO is aldosterone
resistance, aldosterone deficiency, or a combination of both. As the distal renal tubule is damaged,
it progressively becomes unresponsive to aldosterone stimulation. Aldosterone deficiency occurs as
interstitial renal damage impairs the stimulation of renin secretion, thereby suppressing the reninangiotensin-aldosterone axis.[11]
The diagnosis of UTO begins with the insertion of a bladder catheter; resulting diuresis suggests
obstruction below the bladder. If catheterizing the bladder does not produce diuresis, a renal
ultrasound can be used to confirm hydronephrosis with a sensitivity and specificity of 90%. False
negatives on ultrasonography result from concomitant volume depletion, retroperitoneal
fibrosis, obstructing malignancy, or if imaging is done too soon after the onset of an acute
obstruction.[12] False positives occur in the setting of congenital anomalies and during diuresis.
[13] In the setting of flank pain and suspicion for renal calculus without evidence of renal
impairment, a kidneys-ureters- bladder x-ray will detect approximately 90% of renal stones.[3]
Antegrade and retrograde urography can be used to determine the location of the urinary
obstruction.
The management of UTO is directed by the underlying cause; however, regardless of the cause,
relief of a prolonged period of obstruction with anuria is often accompanied by postobstructive
diuresis. In most cases, this polyuria is transient and may be an adaptive response to fluid overload
from the anuria, possibly compounded by iatrogenic fluid administration prior to the diagnosis
of UTO. Routine monitoring of vital signs and serum electrolytes is important to assess possible
volume depletion or the development of acquired DI.[14] The mechanism of this latter
phenomenon is the same as that of the polyuria of partial UTO, manifesting as hypernatremia
resistant to vasopressin. Alternatively, large sodium losses from tubular dysfunction will result
in hyponatremia. If tachycardia and/or orthostatic hypotension develop following relief of the
obstruction, pathologic hypovolemia secondary to diuresis and tubular damage should be
suspected. In either of these instances, fluid and electrolyte correction are warranted; otherwise,
fluid administration may only be serving to prolong the diuretic phase of the postobstructive
recovery.[3,14]
The prognosis for the recovery of renal function is dependent upon the severity and duration of the
obstruction. In addition, patients with obstruction complicated by pyelonephritis generally have a
much worse outcome. Longstanding UTO leads to tubulointerstitial damage, which can ultimately
result in ESRD. In the pediatric population, congenital urologic anomalies causing obstruction are
the major cause of ESRD requiring dialysis.[15] With the exception of these risk factors, there is no
way of accurately predicting to what degree renal function will be restored after an
obstruction is removed.

Following relief of the urinary obstruction, hemodynamic stabilization, and treatment of electrolyte
abnormalities, the next step is monitoring. The follow-up labs should include measurement of
serum creatinine to assess renal function in an effort to guide treatment following the initial
management of BPH.
Monitoring of patients for symptoms of worsening BPH, which could result in a repeat UTO, is
essential. Clinicians should be vigilant of herbal and over-the-counter medication use in patients
with BPH, as some of these can lead to urinary retention with UTO.[16]
In the case presented, a Foley catheter was initially inserted, 2200 mL of urine were emptied, and
the catheter was clamped. An hour later, 1700 mL were drained and the catheter was again clamped.
A third drainage 50 minutes later yielded another 1000 mL. In total, 4900 mL of red-tinged urine
was drained. The patient's abdominal distention promptly resolved with evacuation of the bladder,
and the lower extremity edema regressed over the course of the patient's 4-day hospital stay. A
review of the literature yielded case reports of similarly exaggerated urinary retention, including
one case of a patient retaining more than 16 L over a 10-day period of anuria.[17] The patient's
creatinine levels dropped dramatically by the time of discharge and were within the normal
reference range on follow- up 1 week after discharge.

Medscape
CME
Presentations

Case

A 38YearOld Woman with Abdominal Pain and

a Palpable Mass
Figure
1.

Figure
2.

A 38yearold woman presents with a 2year history of an abdominal wall mass that has
recently enlarged in size. She reports unusual sensations of soreness and pain in her
abdomen associated with the mass. The symptoms are predominantly premenstrual and
have progressed to the point of debilitation. She has not noticed any other masses or
lesions on her body. Three years prior to
presentation, the
patient began
experiencing menorrhagia and dysmenorrhea.
The patient's gynecologic history is significant for menarche at 10 years of age, an
elective abortion at age 18, and an ectopic pregnancy treated by left salpingectomy at
age 25. She has never taken hormonal contraception. She underwent ovarian stimulation
and uterine preparation for in vitro fertilization (IVF) at age
25. Ovarian stimulation was achieved with progesterone and leuprolide acetate
and was followed by
laparoscopic retrieval of her ova. The patient later had 4 transvaginal IVF embryo
transfers resulting in 3 pregnancies and 4 children. Her first 2 children were born via
normal spontaneous vaginal deliveries when the patient was 26 and 28 years old. At
age 30, she gave birth to twins, one via normal spontaneous vaginal delivery and the
other via cesarean because of failure to progress.
She has had no other surgeries. She has no other significant medical history. She denies
any allergies and, at presentation, she is not on any medications. She denies any recent
weight loss, fevers, or chills.
On initial examination, her temperature is 97.6F (36.4C), blood pressure is 126/83 mm
Hg, heart rate is 67 beats/min, respiratory rate is 12 breaths/min, and oxygen saturation

is 99% on room air. She has a firm, nonmobile, nonpulsatile, illdefined, tender mass
palpated to the left of her umbilicus. The mass is not in the area of her prior incisions.
The remainder of her examination, including the pelvic examination, is unremarkable.

The preoperative laboratory findings are within normal limits. An MRI demonstrates a 3.2
2.4 1.8 cm mass within the left abdominal rectus muscle, which deforms the
posterior rectus fascia. The radiologic features are interpreted as being most compatible
with abdominal wall fibromatosis. Intraoperatively, the mass is excised from within the
musculature of the rectus without disturbing the posterior rectus fascia. Grossly, the
mass is found to be 3.7 3.3 1.4 cm and composed of tanyellow, soft, lobular, fibrous
adipose tissue. Histologic sections are shown (Figures 1 and 2).

What is the most likely

diagnosis?
Hint:
The
pain
premenstrual.
A.
B.
C.
D
.

is

Discuss
ion
The diagnosis of endometriosis was made after surgical excision on the basis of the
patient's history and histologic findings. Typical for endometriosis, the patient's pain
increased immediately before and during her menses. However, she did not recall a prior
history of endometriosis. Endometriosis is definitively diagnosed at surgery. It was not
noted at this patient's prior pelvic surgeries. An MRI demonstrated findings consistent
with an abdominal wall fibromatosis; grossly, the tumor appeared similar to a lipoma.
The diagnosis was not confirmed until histologic sections were obtained. The histologic
sections showed irregular endometrial glands and stroma interspersed within muscular
and other soft tissue (Figure 1). The glands were lined by columnar epithelium
surrounded by endometrial stromal tissue. There was evidence of hemorrhage and
hemosiderin laden macrophages, consistent with menstrual cycle changes (Figure 2).
The presence of cholesterol clefts and giant cells also suggested past hemorrhage. The
glandular tissue was estrogenreceptor positive, further supporting a uterine endometrial
origin. On the basis of the typical histologic appearance, the diagnosis of endometriosis
was made.
First described in 1860, endometriosis continues to be a benign but debilitating disease
that burdens millions of women each year. Pelvic endometriosis is the presence of
endometrial glands and stromal tissue outside of the uterine cavity but confined to the
pelvis. Extrapelvic endometriosis refers to endometrial tissue found anywhere in the
body outside of the pelvic cavity.[1,2] Although the pathophysiology of endometriosis
is poorly understood, several theories have been proposed.
The first and best supported is the implantation theory, which suggests that endometrial
tissue passes through the fallopian tubes in a retrograde fashion to attach and
proliferate at ectopic sites in the peritoneal cavity. This theory has been observed in
menstruating females during laparoscopic surgery, as well as in animal models
mimicking retrograde flow. These studies have not only demonstrated retrograde flow,
but they support the idea that sloughed endometrial cells can reimplant and survive
outside the pelvic cavity.[3] A second proposed theory is the direct extension theory,
which states that endometriosis results from direct invasion of ectopic endometrium
through the uterine musculature. However, studies have thus far failed to show a
connection between direct invasion and ectopic endometrial implants.[3] A third theory,
the lymphatic/vascular metastases theory, suggests that endometrial cells can
metastasize through lymphatic and hematogenous routes. This theory has been
supported by a few studies demonstrating endometrial tissue in pelvic lymph nodes and
findings of endometrial tissue in uterine blood vessels.[3] Other theories have also
been proposed, but the majority of evidence seems to support the implantation theory.
It is estimated that there is a 10% prevalence in the general population and that the
condition is the third leading cause of gynecologicrelated hospitalization.[4] In 2002, it
was estimated that medical and surgical treatment of this disease cost $22 billion.[5]
However, the true prevalence of endometriosis is most likely underestimated, as the
disease can be asymptomatic or manifest only minimal symptoms and can be difficult to
diagnose without incidental discovery during surgery.[2]
Several clinical features are commonly seen in patients with endometriosis, including an
age between 30 and

40 years, nulliparity, and involuntary infertility. They also may have dysmenorrhea,
dyspareunia, and the classic symptom, pelvic pain.[2] Pain and infertility are the most
common sequelae of this disease and can cause devastating effects on the physical,
mental, and social wellbeing of affected women.[6]

Due to a lack of sufficient studies, the true prevalence of extrapelvic

endometriosis remains unknown. Extrapelvic endometriosis has been reported in the
gastrointestinal tract,[7] appendix,[8] inguinal canal,[9] liver,[10] lung,[11] umbilicus,
[12] cesarean scar,[13] and rectus abdominus.[1] Cases have also been reported of
abdominal wall endometriosis following needle introduction from amniocentesis.[14,15]
Recently Blanco and colleagues[16] noted a 4% prevalence of abdominal wall
endometriosis in a retrospective study of 297 patients with endometriosis. Common
clinical symptoms for these cases of endometriosis included a palpable mass,
dyspareunia, menorrhagia, and dysmenorrhea.
An initial workup of possible extrapelvic endometriosis should include a detailed history
and physical examination, various imaging modalities, and/or fineneedle aspiration
(FNA). The differential diagnosis of these abdominal wall masses on presentation should
include abscess, lipoma, hematoma, epithelial inclusion cyst, suture granuloma, hernia,
desmoid tumor, sarcoma, lymphoma, and primary or metastatic cancer.[17]
FNA will demonstrate the tubular and spindleshaped stromal cells seen in
endometriosis. Endometrial glands with endometrial stroma can also be appreciated
on
hematoxylineosin stained
specimens.[17] Imaging modalities include
ultrasonography, CT, and MRI of masses. Classic endometriosis will show lowlevel
homogeneous internal echoes on ultrasound that can be demonstrated 95% of the time.
[18] CT scanning of these masses is nonspecific, with findings including simpleto
complex cystic structures and contrast enhancement due to vascularity and hemorrhagic
components.[19] MRI is the most specific modality because it can detect hemorrhagic
nodules containing degenerated blood product, with T2weighted images showing
progressive loss of signal in the dependent portion of the lesion as a result of
accumulation of chronic blood products from cyclic bleeding.[20]
The mainstay of treatment for endometriosis includes medical and/or surgical treatment.
[6] Medical therapies consist of the use of progestogens, oral contraceptive pills, GnRH
agonists, and androgens (although these are rarely used because of their sideeffect
profile). Sustained progestins work by atrophying the glands, while GnRH analogs
suppress endogenous estrogen. Surgical procedures can be performed either as
firstline management or when refractory to medical therapy. Treatment options include
laparoscopic or open excision, fulguration, or laser ablation of endometriosis, resection of
rectovaginal nodules, lysis of adhesions, and interruption of nerve pathways.[21]
Recurrence of symptoms is common in up to 60% of patients, and postoperative
medical therapy is normally continued with a GnRH agonist, danazol, or combined oral
contraceptives.[21]
The role of IVF leading to worsening of endometriosis is currently being studied and is
controversial in nature. It is unclear whether ovarian stimulation leads to
progression of disease in these patients due to the unopposed estrogen. Although
there have been no prospective controlled trials regarding this topic, several case reports
and retrospective studies have presented data for both sides of the argument.[2225]
Most recently, in a review article by Dechaud and colleagues,[26] the authors conceded
that more data need to be obtained to conclusively determine whether IVF plays a role in
the worsening of endometriosis.

In this case, the patient had no known history of endometriosis yet still developed
endometriosis. This emphasizes that a detailed patient history is essential when
compiling a differential diagnosis. Although endometriosis was an unlikely diagnosis
based on her medical history alone, it was only with detailed questioning of the
signs and symptoms that this diagnosis was suspected prior to surgery. The
patient underwent surgery without complications and was discharged to home the
same day. She has done well

postoperatively and is painfree. Because she had an isolated nodule and no other
symptoms or signs of endometriosis were seen on previous laparoscopies, she remains
off medical therapy.
CME Test
A 36yearold woman presents with a palpable mass directly underneath a prior
cesareandelivery scar. She states that she has a history of endometriosis and has
noticed that the mass becomes larger and more painful with her menses. Which
preoperative test is the most specific modality for the diagnosis of
endometrioma?
A. Ultrasound
B. Fineneedle aspiration
(FNA) C. CT scan
D. MRI
A 32yearold woman presents to your office stating that she cannot get pregnant after
trying for 2 years. You attempt to elicit a more complete history to determine whether
she could possibly have endometriosis. Which of the following conditions, should
they be part of her history, is a likely symptom of endometriosis?
A. Dysuria
B. Weight gain
C. Dysmenorrhea
D. Breast tenderness