Caso 24 2016NEJMcpc1503829

T he new engl and jour nal of m e d i cin e
Case Records of the Massachuset ts Gener al Hospital
Founded by Richard C. Cabot

Eric S. Rosenberg, M.D., Editor Nancy Lee Harris, M.D., Editor
Jo-Anne O. Shepard, M.D., Associate Editor Alice M. Cort, M.D., Associate Editor
Sally H. Ebeling, Assistant Editor Emily K. McDonald, Assistant Editor
Case 24-2016: A 66-Year-Old Man

with Malaise, Weakness, and Hypercalcemia
Hasan Bazari, M.D., William E. Palmer, M.D., Jason M. Baron, M.D.,
and Katrina Armstrong, M.D.
Pr e s e n t a t io n o f C a s e
Dr. Shruti Gupta (Medicine): A 66-year-old man was admitted to this hospital known, the patient was
because of malaise, weakness, and hypercalcemia. contacted and asked to
Thirty-f ive hours before admission, the patient was seen in an outpatient return the next day for
clinic aff iliated with this hospital for evaluation of multiple problems, additional testing.
including a
3-week history of mild pain in the shoulder and left side of the neck, a 2-month
history of muscle pain in the left leg that had occurred after a sports injury, list-
lessness, and a 3-month history of increasing frequency of urination, which oc-
curred in small amounts up to twice each night and every 3 hours during the
day and for which he had begun to restrict f luid. His neck pain had developed at
work. Examination of the neck had revealed trapezius muscle spasm; naproxen,
acetamin- ophen, and cyclobenzaprine had been administered, and the pain
partially decreased.
He also had a history of hypertension, benign prostatic hypertrophy, diverticu-
litis, lumbar disk disease, colonic polyps, ischial bursitis, chronic dyspepsia, noc-
turnal leg cramps, excessive alcohol use, and osteoarthritis of the shoulders,
knees, and hips. Medications were amlodipine, hydrochlorothiazide, aspirin,
calcium carbonate for dyspepsia, tamsulosin, n–3 fatty acids, glucosamine, and
a multi- vitamin, as well as ibuprofen and naproxen for musculoskeletal
symptoms and, as needed, tadalaf il and disulf iram. He had no known
medication allergies.
On examination, the patient appeared to be comfortable. The temperature was
36.7°C, the blood pressure 120/80 mm Hg, the pulse 108 beats per minute,
and the body-mass index (the weight in kilograms divided by the square of the
height in meters) 31.2. The posterior neck and occipital region on the left side
were ten- der but had full range of motion, and the remainder of the
examination was normal. The platelet count, red-cell indexes, and blood levels of
glucose, thyrotro- pin, aspartate aminotransferase, and alanine
aminotransferase were normal; other test results are shown in Table 1.
Examination of the urine revealed turbid yellow f luid that was otherwise normal;
urine culture was negative. That evening, after results of the blood tests were
n engl j med 375;6 nejm.org August 11, 5

The New England Journal of
Medicine
Downloaded from nejm.org by ADRIANA PATRICIA STEREN on August 13, 2016. For personal use only. No other uses without
From the Departments of Medicine (H.B., K.A.), Radiology (W.E.P.), and Pathol- ogy ( J.M.B.),
Massachusetts General Hos- pital, and the Departments of Medicine (H.B., K.A.), Radiology (W.E.P.), and
Pa- thology ( J.M.B.), Harvard Medical School
— both in Boston.
N Engl J Med 2016;375:567-74. DOI: 10.1056/NEJMcpc1503829

Copyright © 2016 Massachusetts Medical Society.
n engl j med 375;6 nejm.org August 11, 5

Medicine
Table 1. Laboratory Data.*
8 Mo before 35 Hr before 9 Hr before

Reference Range, Admission, Admission, Admission, On
Variable Adults† Outpatient Clinic Outpatient Clinic Outpatient Clinic Admission
Hematocrit (%) 41.0–53.0 (men) 35.9 36.1 34.4
Hemoglobin (g/dl) 13.5–17.5 (men) 12.2 12.1 11.7
White-cell count (per mm3) 4500–11,000 7200 7400 8200
Differential count (%)
Neutrophils 40–70 66.6 73.2
Lymphocytes 22–44 17.8 14.3
Monocytes 4–11 8.8 6.7
Eosinophils 0–8 6.4 5.2
Basophils 0–3 0.4 0.4
3
Erythrocyte count (per mm ) 4,500,000– 3,940,000 3,880,000 3,770,000
5,900,000
Erythrocyte sedimentation rate (mm/hr) 0–13 33
Sodium (mmol/liter) 135–145 141 141 143 139
Potassium (mmol/liter) 3.4–4.8 3.8 4.5 4.3 3.8
Chloride (mmol/liter) 100–108 103 99 98 98
Carbon dioxide (mmol/liter) 23.0–31.9 25.4 30.8 25.4 32.5
Plasma anion gap (mmol/liter) 3–15 13 11 20 9
Urea nitrogen (mg/dl) 8–25 19 46 49 49
Creatinine (mg/dl) 0.60–1.50 1.50 4.17 5.39 5.06
Estimated glomerular filtration rate ≥60 47 14 10 11
(ml/min/1.73 m2)‡
Calcium (mg/dl) 8.5–10.5 9.6 13.9 16.9 15.0
C-reactive protein (mg/liter) <8.0 16.5
Ionic calcium (mmol/liter) 1.14–1.30 1.79
Venous blood gases§
Fraction of inspired oxygen Not specified
pH 7.30–7.40 7.47
Partial pressure of carbon dioxide (mm Hg) 38–50 36
Partial pressure of oxygen (mm Hg) 35–50 163
Base excess (mmol/liter) 2.2
* To convert the values for urea nitrogen to millimoles per liter, multiply by 0.357. To convert the values for creatinine to micromoles per liter,
multiply by 88.4. To convert the values for calcium to millimoles per liter, multiply by 0.250. To convert the values for ionic calcium to milli-
grams per deciliter, divide by 0.250.
† Reference values are affected by many variables, including the patient population and the laboratory methods used. The ranges used at
Massachusetts General Hospital are for adults who are not pregnant and do not have medical conditions that could affect the results.
They may therefore not be appropriate for all patients.
‡ If the patient is black, multiply the result by 1.21.
§ Venous blood gas measurements were obtained 8.75 hours after admission.
Approximately 26 hours after the initial labo- ferase, and aspartate aminotransferase were
ratory tests, the additional testing was normal; other test results are shown in Table 1.
performed. The blood levels of glucose, total Eight hours later, when the test results were
protein, albumin, globulin, total bilirubin, known, the patient was advised to go to the
lactate dehydroge- nase, alkaline phosphatase, emergency department of this hospital for
alanine aminotrans- evalu-
568 n engl j med 375;6 nejm.org August 11, 2016

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C a se R ecor ds of the M a ssachuse t t s Gener a l Hospita l
ation of potentially life-threatening abnormali- sclerotic lesion involving the right eighth rib
ties, and he was subsequently admitted. (Fig. 1). A radionuclide bone scan was
In the emergency department, the patient re- recom- mended as a screening study for
ported residual stiffness of the neck. He had additional skele- tal lesions. The bone scan
had an inf luenza-like illness (with subjective revealed nonspecif ic abnormal uptake by the rib
fevers, diaphoresis, and nasal congestion) lesion and at the left ischium (Fig. 2). Because
approximately 3 weeks before this evaluation there were concerns about cancer, magnetic
that resolved spontaneously, and he reported resonance imaging (MRI) of the pelvis was
chronic constipation that was unchanged. He recommended for further evaluation and
had stopped drinking alcohol 4 years earlier revealed a high-grade tear of the
and did not smoke tobacco or use illicit drugs.
He lived with his wife, had adult children, and
worked in an off ice. His father and a
grandfather had died of lung cancer, a
grandmother had died of a stroke, his mother
had died of liver disease, and an uncle had
had pancreatic cancer.
On examination, the temperature was 36.8°C,
the blood pressure 159/114 mm Hg, the
pulse
109 beats per minute, the respiratory rate 20
breaths per minute, and the oxygen saturation
97% while the patient was breathing ambient
air. The remainder of the examination was nor-
mal. An electrocardiogram showed sinus rhythm Figure 1. CT Scan of the Chest.
with a ventricular rate of 101 beats per A CT scan of the chest, obtained on hospital day 1,
showed an indeterminate sclerotic lesion located at
minute, a PR interval of 260 msec, a QRS
the anterolateral aspect of the right eighth rib
complex of (arrow).
136 msec, and a ratio of QT interval to QT in-
terval corrected for heart rate of 318:412
msec; f irst-degree atrioventricular block and
right bundle-branch block were present and
had not been present 3 years earlier. A chest
radiograph showed clear lungs and degenerative
changes of the spine. The platelet count,
prothrombin time, and prothrombin-time
international normalized ratio were normal, as
were blood levels of glucose, phosphorus,
lactic acid, magnesium, total protein, albumin,
globulin, total and direct bilirubin, alkaline
phosphatase, alanine aminotransferase,
aspartate aminotransferase, lipase, troponin T,
and N-terminal pro–B-type natri- uretic peptide;
other test results are shown in Table 1.
Urinalysis revealed yellow, slightly cloudy urine,
with a pH of 9.0, a specif ic gravity of 1.006,
and 1+ occult blood by dipstick, as well as 0 to 2
red cells and 3 to 5 white cells per high- power f Figure 2. Radionuclide Bone Scan.
ield; squamous cells were present. The patient A radionuclide bone scan, obtained on hospital day 2,
showed abnormal uptake of the radiotracer by the rib
was admitted to the hospital, and additional lesion (not visible in this image). This nonspecific up-
imaging studies were obtained. take could be explained by trauma or metastatic
Dr. William E. Palmer: Computed disease. On a posterior view of the pelvis, a second
tomography (CT) of the abdomen and pelvis, focus of abnormal uptake involved the left ischium
performed without the administration of (arrow).
intravenous or oral contrast material, revealed
no evidence of can-
Medicine
cer. CT of the chest revealed an indeterminate
n engl j med 375;6 nejm.org August 11, 2016 569

Medicine
left common hamstring tendon at the ischial diseases, such as tuberculosis and sarcoidosis,
tuberosity attachment site. A f also cause tubulointerstitial disease and hyper-
luoroscopically guided glucocorticoid injection calcemia through an increase in the 1-
had been performed at this location 11 hydroxyl- ation of 25-hydroxyvitamin D.
months earlier. Postrenal kidney injury may occur in a patient
Dr. Gupta: Additional tests were performed, with extrinsic compression of the ureters by a
and a diagnosis was made. tumor, which also may cause hypercalcemia.
Di f f e r e n t i a l Di a g n o s i s Hypercalcemia
In addition to acute kidney injury,
Dr. Hasan Bazari: I am aware of the diagnosis hypercalcemia was present in this patient. The
in this case. A recommended approach to differential diagnosis for hypercalcemia is
clinical reasoning is to f irst construct a extensive and includes many uncommon
comprehensive list of the problems and to then diseases, as well as several conditions that
select the key features of the presentation to are investigated even though they are
create a more focused representation of the associated with a low pretest probability because
problems.1 In this case, a 66-year-old man had they can lead to devastating outcomes if they go
hypertension, recent upper respiratory infection, untreated. Among patients with hyper-
a 3-week history of shoulder and neck pain, calcemia who present to the emergency depart-
listlessness, urinary frequency, and ment, the most common cause is cancer, which
constipation and was found to have anemia, accounts for 35% of cases.4 Cancer causes
acute kidney injury, and hypercalcemia. A hypercalcemia through a variety of
differential diagnosis is created for the most mechanisms, including elaboration of
notable problems, which, in this patient, are parathyroid hormone–related protein in many
acute kidney injury and hypercalcemia. solid tumors, excess production of 1,25-
dihydroxyvitamin D in some patients with
Acute Kidney Injury lymphoma, and osteolytic bone lesions in
This patient presented with acute kidney injury; persons with multiple myeloma or cancer that
his creatinine level was 5.06 mg per deciliter metastasizes to bone. However, before we ref
(447 μmol per liter) on admission, as compared lex- ively focus our thinking and diagnostic
with a level of 1.50 mg per deciliter (133 resources on such diagnoses as cancer, we
μmol per liter) at baseline, measured 8 months should care- fully review the history and the
earlier. In order to determine the cause of this initial results of basic laboratory tests to
change in renal function, I will focus on determine whether as- pects of the patient’s
possible pre- renal, intrarenal, and postrenal presentation might suggest an alternative
mechanisms of kidney injury and will explanation for his hypercalcemia and thus
especially consider diseases that result in both obviate the need for an extensive search for
acute kidney injury and hypercalcemia. cancer.
Patients with hypercalcemia often have pre-
renal azotemia in addition to volume depletion Clues from the Case History
due to poor oral intake, natriuresis, and a con- and Laboratory Data
centration defect in the kidney due to down- Are there any clues from this patient’s history
regulation of the expression of aquaporin-2, a that may point us toward the diagnosis? This
molecule that is critical in the reabsorption of patient’s medication history includes nonste-
water in the kidney.2 In considering intrarenal roidal antiinf lammatory drugs (NSAIDs),
causes of acute kidney injury, vascular and glo- hydro- chlorothiazide, and calcium carbonate,
merular diseases are not often associated with which he used for dyspepsia. The patient should
hypercalcemia, although hypercalcemia has been be asked to provide information about his use of
reported in patients with granulomatosis with calcium carbonate, including dosage, frequency,
polyangiitis.3 Several tubulointerstitial time of day, the circumstances under which
diseases are associated with hypercalcemia, he might take more or less, and duration.
including multiple myeloma, which is an Detailed clarif i- cation of the medication
attractive diagnosis in this patient because of history with patients, families, and pharmacies
the indeterminate sclerotic lesion involving the is important in com- piling a complete history
rib that was seen on the CT scan of the for all patients but is especially critical for a
chest. Granulomatous patient presenting with hypercalcemia.
Medicine

Medicine
Are there any clues from this patient’s With a presumptive diagnosis of the milk
laboratory test results that may inform our
differential diagnosis? The elevated bicarbonate
level and the urinary pH of 9 suggested
metabolic alkalosis, which was conf irmed with
the venous blood gas measurement.
After careful review of the history and
results of basic laboratory tests, we can
reframe the representation of the problems:
this 66-year-old man had hypertension while he
was receiving hydrochlorothiazide, recent upper
respiratory infection, dyspepsia for which he
had received long-term treatment with calcium
carbonate, a
3-week history of shoulder and neck pain for
which he had received treatment with NSAIDs,
listlessness, urinary frequency, constipation,
acute kidney injury, metabolic alkalosis with a
high urinary pH, and hypercalcemia. This
reconf ig- ured representation highlights the
combination of hydrochlorothiazide, NSAID
use, and hypercalcemia as an explanation for
the patient’s acute kidney injury. The
uncommon combination of metabolic alkalosis
and hypercalcemia strongly suggests the milk
alkali syndrome as the cause of the
hypercalcemia.5
Milk Alkali Syndrome

The milk alkali syndrome is caused by increased
calcium and alkali intake and is exacerbated by
the intake of hydrochlorothiazide, which pro-
motes calcium reabsorption and generation of
bicarbonate.6 Alkalosis and hypercalcemia are
physiologically synergistic, and the presence of
one condition perpetuates the other. Metabolic
alkalosis increases calcium transport through
the TRPV5 channel and decreases sodium–
potassium–chloride transport in the thick
ascend- ing limb.7
The milk alkali syndrome was originally de-
scribed after milk and alkali were used in com-
bination as a new therapy for ulcer disease.8 The
entity disappeared with the widespread use of
H2-histamine–receptor blockade and proton-
pump
inhibitors, which have replaced milk and
alkali
in the treatment of peptic ulcer disease. How-
ever, widespread use of calcium and vitamin D
supplementation for the treatment of osteoporo-
sis has led to a resurgence of the milk alkali
syndrome. In a 2005 case series examining the
causes of hypercalcemia, the milk alkali syn-
drome caused 8.8% of all cases and 25.7% of
severe cases.9

Medicine
alkali syndrome, the clinician can syndrome, which was exacerbated by the use of
use an often- overlooked hydrochlorothiazide and NSAIDs. I would
diagnostic tool in clinical recommend clarifying the medication history
reasoning: the natural history of with the patient and family, as well as
the disease when medications administering aggressive hydration with normal
are withheld. If hypercalcemia saline and withholding calcium,
resolves while the patient is hydrochlorothiazide, and NSAIDs. I would
receiving no medications, then a specif ically avoid administering
hormonal or lytic cause of bisphosphonates, because they could cause
hypercalcemia is ruled out. The hypo- calcemia. If the calcium level does not
few days that are required to resolve to normal, then a more extensive
clarify the diagnosis in this evaluation for the cause of hypercalcemia is
manner must be weighed against warranted.
the risks of a delay in diagnosis. Dr. Eric S. Rosenberg (Pathology): Dr. Gupta,
In addition, in hospitalized what was your clinical impression when you
patients, we often feel pressure initially evaluated this patient?
to perform parallel testing Dr. Gupta: When I initially met this patient,
instead of sequential testing. the clinical team caring for him was very con-
Parallel testing, which is cerned about cancer, and the patient was antici-
performed in an effort to pating an evaluation to f ind out what type
expedite the diagnosis and of cancer he had. Given that metabolic
eliminate uncertainty, is well- alkalosis is an unusual f inding in persons with
intended, but it can lead to acute kidney injury, we considered the
complications of tests or the dis- possibility of the milk alkali syndrome, but the
covery of incidental lesions that patient’s initial medication history did not
require further investigation. support that diagnosis. Fur- thermore, on the
This path leads not only to in- basis of our review of the literature, the degree
creased costs but also to of hypercalcemia was not typical of the milk
increased anxiety for the patient alkali syndrome alone, and therefore, we
and family; I expect parallel thought that the patient’s presentation was
testing was performed in this more consistent with cancer. We were most
case. concerned about multiple myeloma, prostate
In summary, my diagnosis is cancer, lymphoma, and particularly lung cancer
hypercalcemia and acute kidney because of his family history of lung cancer
injury due to the milk alkali in

Medicine
both his father and grandfather. We thought oversight by a physician who

primary hyperparathyroidism was unlikely in the was unaware that the tests had
presence of symptomatic, severe hypercalcemia, been ordered just days earlier. In
and there were no f indings on chest United States hospitals in 2004,
radiographs to support a diagnosis of more than $5 billion was spent
sarcoidosis. on this type of redundant test-
Clinical Diagn
o s is
Hypercalcemia, most likely due to
cancer.
Dr. Hasan Bazari’s Diagno

ses
Hypercalcemia due to the milk alkali syndrome
and exacerbated by the use of hydrochlorothi-
azide.
Acute kidney injury due to hypercalcemia
and the combination of diuretics and
nonsteroidal antiinf lammatory drugs.
Pa t h ol o g ic a l D i s c u s s
ion
Dr. Jason M. Baron: This patient had extensive
testing as part of the workup for
hypercalcemia and acute kidney injury. The
patterns on serum protein electrophoresis and
urine protein electrophoresis, ratio of kappa
to lambda serum free light chains, and levels
of parathyroid hormone, parathyroid hormone–
related protein, and 25-hydroxyvitamin D
were normal. After the diagnosis of the milk
alkali syndrome was considered, calcium
carbonate was discontinued, and the patient’s
calcium level quickly decreased to within the
normal range. On the basis of these laboratory
f indings, the history of calcium carbonate
antacid ingestion, and the considerations
described in the clinical discussion, the f inal
pathological diagnosis is the milk alkali
syndrome.
The diagnosis of the milk alkali syndrome
can be made with relatively few tests, and one
of the notable features of this case was the
overutilization of laboratory testing. For this
patient, 117 laboratory tests were ordered and
360 results were reported over the course of
two visits to the outpatient clinic and a 3-day
hospital stay. An important driver of test
overutilization in this patient was repeat
testing (both redundant and daily testing). For
example, a second serum protein
electrophoresis was most likely ordered as an
Medicine
ing.10 Duplicate-test alerts are available in some order-entry have accounted for a greater proportion of
systems to help prevent redundant testing.11 Several other the gross domestic product while the rates of
tests were repeated in this case; 7 complete blood counts and 9 achieving key health outcomes have fallen
tests of the phosphorous level were ordered at daily or regu- lar below those of other developed countries.13
intervals, instead of on the basis of a change in the clinical The high cost of health care has been a
situation. Restricting recurrent orders in computerized policy issue for many decades; however, the
order-entry systems or providing alerts that prompt clinicians magnitude of current costs and the recent
to cancel orders that are no longer needed may decrease test economic recession have created a renewed
overutilization.12 sense of urgency. Although much of the
A sequential testing approach may have pre- cluded attention has centered on the role of new
unneeded testing in this patient. How- ever, particularly in models of payment, the success of any effort to
the inpatient setting, the need for a timely diagnosis may increase health care value rests, in the end, on
justify ordering tests in parallel, even when sequential decisions about the use and price of health
testing could lead to a more judicious use of laboratory care interventions.
resources. A health care intervention can be
categorized according to effectiveness and cost
H e a l t h C a r e E c on o m ic s and plotted according to how its cost and
effectiveness com- pare with those of alternative
Dr. Katrina Armstrong: The primary lessons from this case strategies.14 From a population health
focus on the pathophysiological features of hypercalcemia perspective, there is generally agreement that
and the role of the history in the differential diagnosis, but interventions with high cost and low
this case also raises important issues about health care effectiveness should be avoided, but there is
resource utilization and value. The value of health care, def often debate about the use of interventions with
ined as health care outcomes achieved per dollar spent, has lost cost and low effectiveness or those with
gained increasing national attention, because health care costs

Medicine
high cost and high effectiveness. This case re- Dr. Bazari: In one series of 125 patients, the
minds us that opportunities to increase health
care value are available through interventions
with low cost and high effectiveness, such as
detailed history taking, careful analysis of the
initial laboratory values, and the passage of
time. As this case demonstrates, the tendency
to perform parallel testing rather than
sequential testing has increased during
recent years, as the pressure to discharge
inpatients quickly has grown. However, the
effort to reduce the expense of hospital stays
may paradoxically be driving up the cost of the
overall admission, at least in part because tests
often beget more tests.
In the end, we can increase health care value
by adhering to some of the greatest traditions of
internal medicine. These include listening to our
patients and their families, paying close atten-
tion to the available data, and understanding
when to wait.
Dr. Rosenberg: Dr. Gupta, would you tell us
what happened with this patient?
Dr. Gupta: The patient received aggressive
hydration and subcutaneous calcitonin, and
hydrochlorothiazide and calcium carbonate
were discontinued. The initial evaluation for
cancer was unrevealing, and we reconsidered
the possibility of the milk alkali syndrome.
During subsequent discussions with the patient
and his wife, we learned that there was a
marked increase in the amount and frequency
of calcium carbonate he ingested because of
worsening dyspepsia. In addition, he had
recently begun taking over-the- counter
calcium with vitamin D as a supplement for
bone health. During the 3-day hospital stay,
the serum calcium level returned to normal, the
serum creatinine level stabilized, and his malaise
and polyuria resolved. He was discharged home
with strict instructions to avoid calcium
carbonate, ibuprofen, and naproxen. At follow-
up 2 months later, the serum creatinine level
had decreased to
1.34 mg per deciliter (118 μmol per
liter).
A Physician: I participated in the care of
this patient. Although we considered his
calcium carbonate intake, our review of the
literature showed that the milk alkali syndrome
alone would be unlikely to cause a calcium
level of
16 mg per deciliter (4 mmol per liter). How
would you suggest incorporating that informa-
tion into the pretest probability for the milk
alkali syndrome in this case?
Medicine
milk alkali syndrome accounted absolutely en- sured, it is often more
for 9% of cases of hypercalcemia pragmatic to evaluate patients for such
but 26% of cases of severe diagnoses during the hospi- talization.
hypercalcemia.9 However, in Dr. Palmer: I doubt there is one best answer
most instances, a second to your question. Some imaging f indings are
mechanism contributed to either truly indeterminate and require further
renal injury or hypercalcemia. In investigation to rule out cancer. We practice
this patient, the con- current use medicine in an environment that promotes
of a thiazide most likely defensive decision making. Therefore, some
contributed to the level of radiologists recommend additional imaging
hypercalcemia. There may also be studies to further character- ize a suspicious
some genetic variability in the lesion. No one wants to miss an important
absorption and excretion of diagnosis. As an unintended conse- quence,
calcium. one study begets another study, as in this
Dr. Muthiah Vaduganathan case. The chest CT revealed a sclerotic lesion
(Medicine): Through- out the that led to a bone scan and then to MRI.
discussion, we have learned a Unfor- tunately, these additional tests may have
great deal about the milk alkali added expense without adding value and created
syndrome and judicious use of anxiety for the patient and his family. Direct
laboratory testing, but we have com- munication among physicians may help
not dis- cussed the approach to to put incidental and equivocal findings into the
diagnostic imaging in this proper context and obviate unnecessary testing.
patient. Trainees often rely heavily
on radiologists’ Fi n a l D i a g n os
recommendations to perform is
additional diagnostic imaging
studies. When is it appropriate The milk alkali syndrome.
to defer or delay this suggested This case was presented at the Medical Case Conference.
Dr. Bazari reports holding stock in Pf izer; Dr. Baron,
testing, especially when receiving grant support to his institution from International
potentially consequential Business Machines; and Dr. Armstrong, receiving consulting
diagnoses, such as cancer, are fees from GlaxoSmithKline. No other potential conf lict of
interest rele- vant to this article was reported.
being considered? Unless early Disclosure forms provided by the authors are available with
outpatient follow-up can be the full text of this article at NEJM.org.

Medicine
Reference s
1. Bowen JL. Educational strategies to induced severe hypercalcemia: a case re- nating redundant tests: cutting costs in
promote clinical diagnostic reasoning. port and review of literature. Am J Ther U.S. hospitals. Health Aff (Millwood)
N Engl J Med 2006;355:2217-25. 2010;17(6):e234-6. 2009;28:1475-84.
2. Khanna A. Acquired nephrogenic dia- 7. Patel AM, Goldfarb S. Got calcium? 11. Baron JM, Dighe AS. The role of infor-
betes insipidus. Semin Nephrol 2006;26: Welcome to the calcium-alkali syndrome. matics and decision support in utilization
244-8. J Am Soc Nephrol 2010;21:1440-3. management. Clin Chim Acta 2014;427:
3. Jacobs TP, Bilezikian JP. Clinical re- 8. Burnett CH, Commons RR, Albright F, 196-201.
view: rare causes of hypercalcemia. J Clin Howard JE. Hypercalcemia without hyper- 12. Neilson EG, Johnson KB, Rosen-
Endocrinol Metab 2005;90:6316-22. calcuria or hypophosphatemia, calcinosis bloom ST, et al. The impact of peer man-
4. Lindner G, Felber R, Schwarz C, et al. and renal insuff iciency — a syndrome fol- agement on test-ordering behavior. Ann
Hypercalcemia in the ED: prevalence, eti- lowing prolonged intake of milk and al- Intern Med 2004;141:196-204.
ology, and outcome. Am J Emerg Med kali. N Engl J Med 1949;240:787-94. 13. Porter ME. A strategy for health care
2013;31:657-60. 9. Picolos MK, Lavis VR, Orlander PR. reform — toward a value-based system.
5. Berend K, de Vries APJ, Gans ROB. Milk-alkali syndrome is a major cause of N Engl J Med 2009;361:109-12.
Physiological approach to assessment of hypercalcaemia among non-end-stage re- 14. Black WC. The CE plane: a graphic
acid–base disturbances. N Engl J Med nal disease (non-ESRD) inpatients. Clin representation of cost-effectiveness. Med
2014;371:1434-45. Endocrinol (Oxf ) 2005;63:566-76. Decis Making 1990;10:212-4.
6. Desai HV, Gandhi K, Sharma M, Jen- 10. Jha AK, Chan DC, Ridgway AB, Franz Copyright © 2016 Massachusetts Medical Society.
nine M, Singh P, Brogan M. Thiazide- C, Bates DW. Improving safety and elimi-
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shown at the live Clinicopathological Conference (CPC) that is the basis of the Case Record. This slide set contains all of the
images from the CPC, not only those published in the Journal. Radiographic, neurologic, and cardiac studies, gross specimens,
and photomicrographs, as well as unpublished text slides, tables, and diagrams, are included. Every year 40 sets are produced,
averaging 50-60 slides per set. Each set is supplied on a compact disc and is mailed to coincide with the publication of the
Case Record.
The cost of an annual subscription is $600, or individual sets may be purchased for $50 each. Application forms for the current
subscription year, which began in January, may be obtained from the Lantern Slides Service, Department of Pathology,
Massachusetts General Hospital, Boston, MA 02114 (telephone 617-726-2974) or e-mail Pathphotoslides@partners.org.

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T he new engl and jour nal of m e d i cin e

Case Records of the Massachuset ts Gener al Hospital

Founded by Richard C. Cabot

Case 24-2016: A 66-Year-Old Man

n engl j med 375;6 nejm.org August 11, 5

N Engl J Med 2016;375:567-74. DOI: 10.1056/NEJMcpc1503829

n engl j med 375;6 nejm.org August 11, 5

Table 1. Laboratory Data.*

8 Mo before 35 Hr before 9 Hr before

568 n engl j med 375;6 nejm.org August 11, 2016

The New England Journal of

n engl j med 375;6 nejm.org August 11, 2016 569

The New England Journal of

The New England Journal of

Milk Alkali Syndrome

The New England Journal of

n engl j med 375;6 nejm.org August 11, 2016 571

The New England Journal of

both his father and grandfather. We thought oversight by a physician who

Dr. Hasan Bazari’s Diagno

572 n engl j med 375;6 nejm.org August 11, 2016

The New England Journal of

n engl j med 375;6 nejm.org August 11, 2016 573

The New England Journal of

574 n engl j med 375;6 nejm.org August 11, 2016

The New England Journal of

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