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The n e w e ng l a n d j o u r na l of m e dic i n e

Clinical Problem-Solving

CarenG. Solomon, M.D., M.P.H., Editor

A Breakthrough Diagnosis
SaraG. Murray, M.D., RobertM. Wachter, M.D., KerryC. Cho, M.D.,
and Gurpreet Dhaliwal, M.D.

In this Journal feature, information about a real patient is presented in stages (boldface type) to an expert
clinician, who responds to the information, sharing his or her reasoning with the reader (regular type).
The authors commentary follows.

A 19-year-old Palestinian woman with multiple sclerosis presented with altered From the Department of Medicine
mental status, respiratory distress, and abdominal distention after a flight from (S.G.M., R.M.W., K.C.C., G.D.) and the
Divisions of Hospital Medicine (S.G.M.,
Jordan to the United States. Her family reported that she had had progressive short- R.M.W.) and Nephrology (K.C.C.), Univer-
ness of breath and abdominal distention over the previous 2 weeks, followed by in- sity of California, San Francisco (UCSF),
creased confusion during the flight. and the San Francisco Veterans Affairs
Medical Center (G.D.) both in San
Francisco. Address reprint requests to
This patient presents with three urgent problems confusion, abdominal disten- Dr. Murray at UCSF, 533 Parnassus Ave.,
tion, and respiratory compromise. Changes in mental status are usually explained U125, San Francisco, CA 94143-0131, or
at sara.murray@ucsf.edu.
by metabolic derangements, infections (e.g., meningitis or encephalitis), struc-
tural abnormalities (e.g., stroke or tumors), or the effects of toxins or medications. N Engl J Med 2015;373:1865-70.
DOI: 10.1056/NEJMcps1402621
Pathologic abdominal distention reflects the accumulation of liquid (ascites or Copyright 2015 Massachusetts Medical Society.
blood) or gas (caused by an obstruction or perforation). Her respiratory distress
could be the result of a pulmonary condition (e.g., aspiration, infection, or embo-
lism) or of restriction caused by her abdominal distention.

Multiple sclerosis had been diagnosed in Jordan 2 years before this presentation,
when the patient had presented with fatigue, dysphagia, and diplopia. Magnetic
resonance imaging (MRI) of the brain and spine at that time showed findings con-
sistent with multiple sclerosis. An initial response to glucocorticoids was followed by
the development of urinary incontinence, weakness in the left leg, and truncal insta-
bility, all of which were poorly responsive to treatment (which included glatiramer
acetate, interferon, azathioprine, and mitoxantrone). The patient was now wheel-
chair-bound. She also had a history of asthma since childhood, uveitis that was diag-
nosed within the past several years, and chronic anemia. She had been hospitalized in
Jordan 3 weeks before this presentation for a urinary tract infection with Escherichia coli,
which was treated with intravenous antibiotics.

A residual focus of E. coli (e.g., an infected stone or a small renal abscess) may
cause recurrent systemic infection. Chronic anemia could be explained by iron
deficiency, chronic inflammation, the side effects of medication, or thalassemia.
Given its chronicity, the uveitis is unlikely to be related to infection and probably
reflects an associated autoimmune condition such as sarcoidosis, Behets disease,
or a spondyloarthropathy. Consideration should be given to conditions that mimic
multiple sclerosis, including neuromyelitis optica (characterized by the combination
of optic neuropathy and transverse myelitis), which tends to have a more fulminant
course, or demyelination associated with an underlying autoimmune condition,

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The n e w e ng l a n d j o u r na l of m e dic i n e

such as systemic lupus erythematosus, sarcoid- potassium 6.4 mmol per liter, chloride 97 mmol
osis, or Behets disease. per liter, bicarbonate 13 mmol per liter, blood
urea nitrogen 97 mg per deciliter (35 mmol per
The patient was cachectic and in respiratory dis- liter), creatinine 6.3 mg per deciliter (557 mol per
tress. On physical examination, the temperature liter), and glucose 100 mg per deciliter (6 mmol
was 36.8C, the heart rate 139 beats per minute, per liter). The total bilirubin level was 4.8 mg per
the blood pressure 115/68 mm Hg, the respiratory deciliter (82 mol per liter; normal range, 0.2 to
rate 26 breaths per minute, and the oxygen satura- 1.3 mg per deciliter [3.4 to 22.2 mol per liter]),
tion 93% while the patient was breathing ambient with a direct bilirubin level of 2.7 mg per deciliter
air. She was confused and unable to follow com- (462 mol per liter; normal range, <0.3 mg per
mands. Her oropharynx was dry, and her pupils deciliter [<5 mol per liter]), the aminotransferase
were equal and reactive. There was no active uve- levels were normal, and the alkaline phosphatase
itis, but the patient had chorioretinal scars in her level was 471 U per liter (normal range, 35 to 95 U
left eye and was unable to close either eyelid com- per liter). The international normalized ratio was
pletely. Mild scleral icterus was present. She was 1.2. The level of ferritin was 2339 g per liter, the
using accessory muscles of ventilation to breathe serum iron level 69 g per deciliter (12 mol per
and had coarse breath sounds in both lungs. On liter), and the transferrin level 116 mg per decili-
cardiovascular examination, tachycardia was de- ter. The transferrin saturation was 42%, and the
tected, without murmurs. Her abdomen was dis- reticulocyte count 23,200 per cubic millimeter.
tended, with mild tenderness and a fluid wave, An electrocardiogram revealed sinus tachycardia.
but there was no rebound or guarding. Her arms A chest radiograph showed a hazy opacity at the
and legs were cool, with 2+ distal pulses and no right medial lung base that was consistent with
edema. Urgent endotracheal intubation was per- aspiration or pneumonia. A urinary catheter
formed to protect the airway. drained 700 ml of cloudy urine. Urinalysis re-
vealed more than 50 white cells per high-power
Although the patient has no known history of field and 11 to 20 red cells per high-power field.
liver disease, she has scleral icterus, and the
fluid wave detected on examination is consistent The patient has a pronounced metabolic acidosis
with ascites. Abdominal distention can cause with an anion-gap of 16; the probable cause is
restrictive pulmonary physiology and respiratory sepsis with systemic hypoperfusion and uremia.
compromise, but abnormal findings on exami- Her low serum sodium level may reflect dehydra-
nation of the lung suggest that parenchymal tion or the syndrome of inappropriate antidi-
dysfunction is causing her respiratory failure. uretic hormone secretion (arising from undefined
The most pressing concern on the basis of the pulmonary or neurologic disease). The concomi-
limited data is that a pulmonary infection (e.g., tant hyperkalemia suggests that adrenal insuffi-
tuberculosis) or an intraabdominal infection ciency should be considered, although the most
(e.g., abscess or pyelonephritis) has led to sepsis, likely explanation for the hyponatremia, hyper-
with multiorgan failure. Given her respiratory kalemia, and pyuria is acute kidney injury result-
distress and tachycardia after a recent plane ing from acute tubular necrosis in the presence
flight and her chronic immobility, pulmonary of urosepsis. Alternative explanations for intra-
embolism should also be considered. renal injury or inflammation, such as glomeru-
lonephritis or tubulointerstitial nephritis, are less
Measurement of arterial blood gases revealed that likely. The copious urine output after the place-
the pH was 7.17, the partial pressure of carbon ment of a urinary catheter suggests that there
dioxide was 41 mm Hg, and the partial pressure may be obstructive renal injury. The multiple
of oxygen was 49 mm Hg while 2 liters of oxygen sclerosis may have led to a neurogenic bladder,
was provided through a nasal cannula. The lactate which may account for the abdominal disten-
level was 1.5 mmol per liter. The white-cell count tion. The elevated levels of bilirubin and alkaline
was 20,200 per cubic millimeter (with 91% neutro- phosphatase point to a cholestatic process,
phils), the hemoglobin level 11.2 g per deciliter, which could reflect an extrahepatic obstruction
and the platelet count 282,000 per cubic millime- (e.g., stone, stricture, or tumor) or intrahepatic
ter. The level of sodium was 126 mmol per liter, cholestasis (e.g., primary biliary cirrhosis, pri-

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Clinical Problem-Solving

mary sclerosing cholangitis, or an effect of medi- ascites albumin gradient (SAAG; calculated by
cation). An infiltrative disorder, such as sarcoid- subtracting the concentration of albumin in the
osis, tuberculosis, lymphoma, or metastatic ascitic fluid from the concentration in the serum,
cancer, could also account for her presentation with a low SAAG classified as less than 1.1 g per
and the rapid deterioration of her condition. deciliter). The patients elevated SAAG suggests
that portal hypertension is responsible for her
Computed tomography (CT) of the head without ascites. However, the markedly elevated white-
the administration of contrast material revealed cell count in the ascitic fluid is more character-
marked loss of parenchymal volume and chronic istic of a bacterial peritonitis that develops after
sinusitis. CT scans of the abdomen and pelvis the perforation of a viscus (e.g., duodenal ulcer)
without the administration of contrast material than of a spontaneous bacterial peritonitis. Be-
showed large-volume ascites with omental nodu- cause the elevated SAAG is generally a reliable
larity, mild hydronephrosis in both kidneys with indicator of portal hypertension, a mixed picture
urothelial thickening of the proximal and middle should be considered, one that involves portal
segments of the ureters, and airspace disease in hypertension (the cause uncertain at this point)
both lungs, which suggests the possibility of and an infectious or malignant process invading
pneumonia, aspiration, or atelectasis (Fig.1). Ab- the peritoneum.
dominal ultrasonography revealed a heteroge-
neous liver parenchyma with an irregular-appear- The general surgery consultants advised nonopera-
ing surface, patent hepatic vasculature, and no tive management. The patient was started on an
focal masses. Diagnostic paracentesis removed empirical regimen of rifampin, isoniazid, pyra-
120 ml of cloudy fluid with a white-cell count of zinamide, and ethambutol for tuberculosis. On
14,300 per cubic millimeter (with 90% neutro- the next day, CT of the chest, abdomen, and pel-
phils) and a red-cell count of 972 per cubic milli- vis, performed after the administration of con-
meter. The level of glucose was 100 mg per decili- trast material, revealed resolution of the lung
ter, lactate dehydrogenase 1480 U per liter (normal consolidation, new mild pulmonary edema, a
range, 102 to 199), albumin less than 1 g per markedly thickened bladder wall with an abnor-
deciliter, and protein 1 g per deciliter. Grams mal outpouching from the bladder dome, and
staining of a specimen of the fluid revealed no mild-to-moderate hydronephrosis. Diffuse nodu-
organisms, and a smear for acid-fast bacilli was larity of the omentum and mesentery was again
negative. The serum albumin level was 2.7 g per noted (Fig.2).
deciliter. Vancomycin, piperacillintazobactam,
and azithromycin were administered along with Thickening of the bladder wall is frequently
3 liters of intravenous normal saline. The patient noted after a distended bladder has been decom-
excreted 3 to 4 liters of urine overnight, and her
serum creatinine level decreased to 1.1 mg per
deciliter (97 mol per liter) 12 hours after her ini-
tial presentation.

The immediate amelioration of severe acute kid-


ney injury is characteristic of either acute prerenal
kidney injury or postrenal obstruction; intra
renal processes resolve more slowly. Although
the CT scan showed only mild hydronephrosis,
it can take a few days for the collecting system
to dilate in response to increased pressure; in
addition, the study was performed after the place-
Figure 1. Hospital Day 1 Computed Tomography
ment of a urinary catheter. (CT) of the Abdomen and Pelvis without the Use
Although the omental nodularity raises suspi- of Contrast Material.
cion of infection (e.g., tuberculosis) or cancer and Large-volume ascites with substantial omental nodularity
may in rare instances occur with sarcoidosis, can be seen (arrow).
these conditions typically produce a low serum

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The n e w e ng l a n d j o u r na l of m e dic i n e

per deciliter (65 mol per liter). The serum cre-


atinine level at this time was 0.8 mg per deciliter
(71 mol per liter). A fungal smear and Grams
staining of specimens of the fluid were negative
for organisms.

The reduction in the leukocyte count in ascitic


fluid is attributable to antibiotic therapy. Since
creatinine freely crosses the peritoneal mem-
brane, serum and peritoneal creatinine levels are
equivalent under normal conditions. In patients
with urinary ascites, the peritoneal level of cre-
atinine should be higher than the serum level.
Figure 2. Hospital Day 2 CT of the Abdomen and The underlying cause of the patients urothelial
Pelvis after the Use of Contrast Material. and peritoneal disease remains uncertain. The ele-
Marked thickening of the urinary bladder is shown vated level of adenosine deaminase increases the
(white arrowhead), with bladder distention despite uri-
likelihood of tuberculosis, although the levels of
nary catheterization. An abnormal outpouching (mea-
suring 4.2 cm by 3.9 cm) from the dome of the bladder this marker may also be elevated in patients
(white arrow) appears to be continuous with the blad- with peritoneal cancer or bacterial peritonitis.
der. Large-volume ascites can also be seen (black ar-
row). Findings on MRI studies of the brain, spine, and
cerebrospinal fluid were consistent with multiple
sclerosis. Tests for aquaporin-4, anti-Ro (SSA),
pressed or after a bout of cystitis, but this find- anti-La (SSB), and antinuclear antibodies were
ing may also reflect a malignant process, chronic negative. Sputum smears for acid-fast bacilli and
infection (e.g., schistosomiasis), or inflamma- a tuberculin skin test were negative, as were tests
tion from the long-term placement of an in- for the human immunodeficiency virus and for
dwelling catheter. In patients with chronic uri- antibodies to strongyloides and schistosomae.
nary obstruction, bladder diverticula can develop The patient continued to have tachycardia and
in response to long-term elevation of intravesic- hypoxemia. A CT angiogram was negative for
ular pressures. The images should be reviewed pulmonary embolism. Her blood white-cell count,
to see whether the outpouching suggests a diver- which had transiently normalized after admis-
ticulum or an exophytic process, either of which sion, rose to 50,400 cells per cubic millimeter. She
could have perforated the bladder and caused continued to have fevers, with temperatures up to
urinary ascites. 39C, despite the administration of broad-spec-
trum antibiotics and antituberculosis therapy.
The urology consultants recommended continued Urine and ascites cultures were positive for ex-
decompression for what was probably a neuro- tended-spectrum -lactamaseproducing E. coli
genic bladder and antibiotic treatment for cystitis. and Candida glabrata. Blood cultures were sterile.
The specimen of paracentesis fluid that had been Piperacillintazobactam was discontinued and
obtained previously was tested for creatinine level, ertapenem and voriconazole were started, but
which was 5.7 mg per deciliter (504 mol per there was no substantial improvement in the pa-
liter); the serum creatinine level at that time was tients condition.
6.3 mg per deciliter. Diagnostic paracentesis was
repeated on hospital day 3 and yielded a hazy yel- The ongoing tachycardia, hypoxemia, and fevers
low fluid with a white-cell count of 4800 per cubic suggest either inadequate source control of the
millimeter (with 72% neutrophils and 20% mono- infection or a noninfectious process, such as
cytes) and a red-cell count of 130 per cubic milli- cancer or autoimmune disease (e.g., vasculitis).
meter. The level of glucose was 94 mg per deciliter Antibody tests for autoimmune disorders that
(5.2 mmol per liter), lactate dehydrogenase 1877 U have protean manifestations in the central ner-
per liter, adenosine deaminase 69 U per liter (nor- vous system, such as systemic lupus erythema-
mal range, <7.6 U per liter), and creatinine 0.7 mg tosus and Sjgrens syndrome, were negative.

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Clinical Problem-Solving

Testing for aquaporin-4 antibody, the pathologic


antibody in neuromyelitis optica, was also nega-
tive. There may be a reservoir of E. coli in the
urinary system as a result of incomplete eradica-
tion, and that infection may have spread to the
peritoneal fluid hematogenously or through a
direct connection between the bladder and the
peritoneum.

The patient underwent exploratory laparotomy.


Widespread adhesions with cloudy peritoneal
fluid and fibrinous exudates were seen (Fig. 3).
The bowel had no obvious defects. Purulent asci-
tes was noted in the right lower quadrant overly-
ing a thickened bladder that adhered to the mes-
entery. On manipulation of the urinary catheter, a
small bladder perforation leaked urine, and this
observation was confirmed with intravesicular Figure 3. Intraoperative Abdominal Findings.
injection of methylene blue. A biopsy specimen of Fibrinous exudate can be seen throughout the abdo-
the omental nodules revealed focal fat necrosis, men (bladder not shown).
and stains for fungi and acid-fast bacilli were
negative.
At a 9-month follow-up visit, the patients con-
Spontaneous bladder perforation, with spillage dition was stable, and she was receiving ongoing
of infected urine into the peritoneal cavity, led to treatment for multiple sclerosis with natalizumab
secondary bacterial peritonitis. The elevated se- and dimethyl fumarate. Her neurogenic bladder
rum creatinine level at presentation may have re- was managed with the use of intermittent straight
flected impaired kidney function or the reabsorp- catheterization, and there was no recurrence of
tion of the creatinine in the ascitic fluid across bladder perforation.
the peritoneal membrane. The placement of the
urinary catheter decreased the volume of urine C om men ta r y
spilling into the peritoneum and relieved the
urinary obstruction but did not eliminate the The patient presented with altered mental status,
source of infection. ascites, acute kidney injury, and respiratory dis-
tress. Her multisystem illness was ultimately at-
After repair of the bladder perforation, the patient tributed to the rupture of her neurogenic bladder
was treated with a 4-week course of antibacterial and the spillage of infected urine into the perito-
and antifungal therapy. The leukocytosis resolved, neal cavity. Exploratory laparotomy was required
and the results of tests of liver function were nor- to diagnose and definitively treat the rupture.
mal. The postoperative course was complicated by The bladder may rupture and leak urine into
aspiration that was attributed to neuromuscular the peritoneal cavity after trauma, surgery, or
weakness and to paralysis of the left vocal cord. radiation. Spontaneous bladder rupture has been
The fevers resolved within 1 week. The patient associated with cystitis, pelvic cancer, dissemi-
was discharged from the hospital 3 weeks after nated tuberculosis, alcohol abuse, outflow ob-
the operation. Cultures of a specimen from omen- struction, and neurogenic bladder.1 More than
tal biopsy were negative for fungi and mycobacte- 80% of patients with multiple sclerosis have
ria. A urodynamic study performed 4 weeks after genitourinary symptoms, ranging from urge in-
discharge showed a neurogenic bladder with very continence to urinary retention.2 In multiple
high urethral sphincter tone, a finding that was sclerosis, outflow obstruction that is caused by
presumed to have led to high bladder pressures a neurogenic bladder and chronic cystitis can
and spontaneous bladder perforation. Cystoure- contribute to rupture.3 Although ascites with an
throscopy confirmed extensive trabeculation. elevated SAAG typically occurs in patients with

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Clinical Problem-Solving

portal hypertension, urinary ascites may also be ploratory surgery when the resulting studies are
associated with an elevated SAAG.4 nondiagnostic and a patient is becoming pro-
Urinary ascites may mimic acute kidney in- gressively ill. Exploratory surgery has been shown
jury, with a pseudo-kidney injury pattern that to be informative in patients with undiagnosed
includes elevated serum creatinine levels, hypo- ascites.11,12 In one report, among 162 patients
natremia, hyperkalemia, and azotemia, all of who underwent exploratory laparoscopy for
which are caused by the equilibration of urine ascites that remained undiagnosed after the use
and plasma across the peritoneal membrane.4-6 of conventional laboratory testing and imaging
A ratio of ascitic fluid to serum creatinine that techniques, the diagnosis was established with
is greater than 1 is diagnostic of an acute intra- laparoscopy in 85% of the patients; the most
peritoneal leak and indicates that urine produc- common diagnosis was peritoneal carcinomato-
tion exceeds the rate of creatinine equilibration sis, followed by tuberculous peritonitis and cir-
across the peritoneum.4,7 Because the infection rhosis.11
and the bladder leak in this patient were sub- Clinicians should consider the possibility of
acute (possibly because of intermittent leakage, spontaneous bladder rupture in patients with
leading to a slow accumulation of ascitic fluid), unexplained ascites and an underlying disease
it is likely that the ascites and serum creatinine that contributes to bladder dysfunction (e.g.,
level had time to equilibrate, resulting in a 1:1 multiple sclerosis, stroke, paraplegia, diabetes,
ratio.2 or cerebral palsy). As our experience with this
This equilibration was only one of several patient shows, when inflammatory ascites wors-
reasons for the delayed diagnosis (which was ens despite the use of targeted antibiotic ther-
made on hospital day 10). The omental nodules apy, exploratory laparotomy can lead to a break-
seen on CT led the clinicians to focus on an in- through diagnosis and can be lifesaving.
traperitoneal infection or cancer. Serial CT scans Dr. Wachter reports receiving fees paid to his institution for
his membership on the board of directors and his service as
did not reveal definitive evidence of bladder chair of the quality committee for IPC Healthcare, receiving fees
rupture. Nondiagnostic imaging results have for serving on advisory boards for and holding stock options in
been reported in other cases.8,9 Cystography is PatientSafe Solutions, Twine Health, EarlySense, QPID Health, and
Amino.com, receiving lecture fees from the Governance Institute
the best test for rupture, but it is likely to be and Optima Health, and receiving fees for developing and pre-
performed only when there is a high clinical senting patient safety educational material from QuantiaMD.
suspicion of rupture. In a case series, the average No other potential conflict of interest relevant to this article was
reported.
time from an inciting incident or initial presen- Disclosure forms provided by the authors are available with
tation to diagnosis was reported to be 5.4 days.10 the full text of this article at NEJM.org.
Although diagnostic paracentesis and abdomi- We thank Marc Mabray, M.D., for providing and interpreting
the abdominal images, Donna Deng, M.D., for her assistance in
nal imaging are the standard methods for evalu- interpreting the urodynamic studies, and Victoria Lyo, M.D., for
ating new ascites, it is advisable to consider ex- the intraoperative photograph.

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