J Am Soc Nephrol 12: S3–S9, 2001
Hypercalcemic Crisis
REINHARD ZIEGLER
Medizinische Universitätsklinik und Poliklinik, Heidelberg, Germany.
Abstract. Hypercalcemia may decompensate from a more or
less chronic status into a critical and life-threatening condition,
hypercalcemic crisis. In the majority of cases, primary hyper-
parathyroidism is the cause; humoral hypercalcemia of malig-
nancy or rarer conditions of hypercalcemia will decompensate
less often. The leading symptoms that characterize the crisis
are oliguria and anuria as well as somnolence and coma. After
a hypercalcemic crisis is recognized, an emergency diagnostic
Hypercalcemic crisis is a condition involving the decompen-
sation of hypercalcemia, which could have existed for longer
periods or could be acute at the first instance of this electrolyte
disturbance. Compensated hypercalcemia is caused by malig-
nancies in 70% of cases, by primary hyperparathyroidism
(pHPT) in 20% of cases, and by other (rarer) conditions in the
remaining 10% (1); the majority of cases of hypercalcemic
crisis are caused by pHPT (2). The disease is then parathyro-
toxic crisis. The following case history should illustrate this
situation (3).
A 42-yr-old woman had experienced episodes of nausea and
stomach pain for approximately 1 yr. Three months before
admission, she felt weak and lost initiative; these symptoms
were related to professional and familial stress. An outpatient
examination revealed increased alkaline phosphatase levels.
Because other liver function test results were normal, the
alkaline phosphatase was thought to be of skeletal origin.
Skeletal scintigraphy demonstrated only nonspecific spots near
the ankles. Further examinations were refused. The patient
developed tiredness, vomiting, weight loss, and dehydration,
and she needed to be admitted to the hospital. Clinical chem-
istry assays revealed extreme hypercalcemia of 5.9 mM, mild
hypokalemia of 3.1 mM, and borderline creatinine and urea
concentrations. Fluid supply for rehydration decreased the cal-
cium concentration only to 5.4 mM; the patient was oliguric.
Three days later, she was transferred to our hospital, presenting
with hypercalcemic crisis. Renal insufficiency and somnolence
were the primary symptoms. From the history of the patient,
previous goiter resection must be noted.
A diagnostic program to exclude causes other than pHPT
was initiated. To decrease the calcium concentrations, the
Correspondence to Dr. Reinhard Ziegler, Medizinische Universitätsklinik und
Poliklinik, Bergheimer Strasse 58, D-69115 Heidelberg, Germany. Phone:
6221-568601; Fax: 6221-56522; E-mail: sekretariat_ziegler@med.
uni-heidelberg.de
1046-6673/1202-0003
Journal of the American Society of Nephrology
Copyright © 2001 by the American Society of Nephrology
program has to be followed either to prove or to exclude
primary hyperparathyroidism. In the first case, surgical neck
exploration is the only way to avoid fatal outcome. The diag-
nostic program should be performed within hours; during this
time, serum calcium should be lowered. Treatment of choice is
hemodialysis against a calcium-free dialysate. Bisphospho-
nates could be useful as adjuvant drugs.
patient received (in addition to intravenously administered
saline solution and furosemide) 300 mg of clodronate admin-
istered intravenously, 100 mg of prednisolone administered
intravenously, and 100 units of calcitonin administered subcu-
taneously. Because diuresis did not begin within 6 h, hemodi-
alysis was performed, using a calcium-free dialysate. After
12 h, arteriovenous hemofiltration was performed for further
lowering of the serum calcium concentrations, and then hemo-
dialysis was repeated. Clodronate (300 mg) administration was
repeated after 12 h, and calcitonin (100 U) was administered
subcutaneously every 4 h.
Meanwhile, the diagnostic procedure led to the diagnosis of
parathyroid toxicosis. There was no evidence for tumoral hy-
percalcemia, and parathyroid hormone (PTH) levels, measured
in a fast assay, were 2.5-fold elevated. Neck surgery was
performed. The patient was asystolic for seconds when anes-
thesia was initiated, but the operation could be performed. A
parathyroid adenoma of 8.3 g was found and removed. Post-
operatively, the patient again became asystolic. Despite all
efforts at resuscitation, the patient could not be revived. An
autopsy revealed nephrocalcinosis and severe myocardial
calcinosis.
Approximately 20 yr ago, there were more reports of hyper-
calcemic crisis (2). It is evident that the current use of earlier
fluid supply for critically ill patients and optimized strategies
for intensive care medicine have made hypercalcemic crisis a
rare event. However, the life-threatening condition requires
rapid action, to avoid a lethal course such as in this case.
Pathophysiologic Features and Clinical Findings
Calcium homeostasis has been a very stable system from
early periods of evolution. Our extracellular fluid, including
the circulation, conserves the calcium content of the primordial
ocean. When life left that ocean to live on land, systems for the
maintenance of optimal calcium concentrations in body fluids
were developed. Calcium was no longer the content of the
surrounding water; it needed to be taken in and conserved from
food. The skeleton had the double tasks of taking up calcium
S4 Journal of the American Society of Nephrology
for stability and acting as a depot for times of poor calcium
supply.
PTH is one of the principal factors in the prevention of
hypocalcemia. By decreasing calcium excretion, increasing
calcium absorption (via calcitriol), and resorbing depot cal-
cium from the skeleton in cases of emergency, it is a major
contributor to normocalcemia. If PTH is autonomously se-
creted in excess, e.g., in pHPT, hypercalcemia develops.
Renal PTH effects are threefold. In addition to the increase
in calcium reabsorption, PTH stimulates phosphaturia. Phos-
phate loss favors an increase in blood calcium levels via the
constancy of the calcium ⫻ phosphorus ion product. Being a
glandotrophic hormone, PTH activates renal 1-␣-hydroxylase
and increases the formation of calcitriol. Normal concentra-
tions of PTH stimulate bone turnover without bone loss,
whereas PTH excess induces bone resorption to an extent that
cannot be compensated for by new bone formation. In this
situation, the released calcium is needed for the prevention of
hypocalcemia and is not recycled into the newly formed bone.
The kidneys act as one of the regulatory elements of calcium
homeostasis by increasing or decreasing calciuria. If calciuria
is abruptly stopped because of renal insufficiency, stored cal-
cium may induce a phase of hypercalcemia until the other
regulatory links have adapted and counter-regulated levels.
Intestinal calcium absorption is increased if higher levels of
calcitriol are present. Whether increased calcitriol concentra-
tions result from hyperparathyroidism or diseases with in-
creased calcitriol formation (sarcoidosis and other diseases)
does not make a difference. With the complexity of malignant
diseases, several mechanisms may lead to hypercalcemia, in-
cluding the paraneoplastic production and secretion of calcit-
riol, the production of PTH-related peptide (PTHrP), and the
production of hypercalcemic cytokines such as interleukin-1,
interleukin-6, tumor necrosis factor-␣, and prostaglandins (4).
In addition to these endogenous causes of hypercalcemia,
exogenous factors may play causative roles. One factor con-
sists of medications that induce hypercalcemia (vitamin D and
its analogs and vitamin A). Another factor involves immobili-
zation of individuals with labile calcium homeostasis. Immo-
bilization reduces the inflow of calcium into the skeletal tissue,
and calcium is released into the circulation. If the homeostatic
capacity of a patient is already under stress because of preex-
isting diseases (severe osteoporosis, acute severe fractures, or
Paget’s disease of the bone), immobilization can be accompa-
nied by hypercalcemia. Furthermore, endocrinopathies can be
accompanied by hypercalcemia. Thyroid hormone in excess
accelerates bone turnover; therefore, severe thyrotoxicosis can
be accompanied by hypercalcemia. Glucocorticoids are in-
volved in calcium homeostasis, with a calcium-lowering activ-
ity (antagonism to PTH). If glucocorticoid levels are acutely
decreased, hypercalcemia can result (acute Addison’s disease
or acute removal of adrenal tumors with hypercortisolism).
All of these conditions have the character of diseases; the
only exception is benign familial hypocalciuric hypercalcemia
(FHH) (5). Because of an inherited defect of the calcium sensor
of parathyroid cells, the inhibitory feedback effects of calcium
on PTH secretion begin only at hypercalcemia. Calciuria is
J Am Soc Nephrol 12: S3–S9, 2001
decreased and contributes to this hypercalcemia. This condi-
tion is a disturbance but not a disease.
Hypercalcemia induces functional disturbances in a group of
organs, which are considered together as the “hypercalcemic
syndrome” (2). Single components are often nonspecific and
are also observed in many other diseases. If several compo-
nents of the syndrome are present, hypercalcemia is suggested
(Table 1). Because serum calcium concentration determina-
tions are not very expensive, they should be performed in cases
with single symptoms and in all cases of the syndrome.
Renal symptoms are polyuria and polydipsia. Diabetes hy-
percalcemicus must be investigated in any case of polyuria,
especially when diabetes mellitus, diabetes insipidus, and tu-
bulopathies have been excluded. Diuresis attributable to hy-
percalcemia is accompanied by potassium loss; hypercalcemia
generally leads to hypokalemia.
Intestinal symptoms are nausea, vomiting, and constipation
more than diarrhea. The secretion of gastric acid and pancreatic
enzymes is increased.
Central nervous system symptoms are less characteristic,
including tiredness, headache, components of an endocrine
psychologic syndrome (e.g., loss of initiative), and depression.
Cardiac symptoms also are nonspecific. The QT interval is
shortened, and tachycardias may be observed. The increased
sensitivity to digitalis is relevant. The mechanism of hyperten-
sion accompanying chronic hypercalcemia attributable to
pHPT is unclear. Chondrocalcinosis (pseudogout) is occasion-
ally observed.
When hypercalcemia reaches a critical level (⬎4 mM), two
organs are at risk for decompensation. Polyuria may develop
into oliguria and finally anuria, especially in case of exsiccosis.
Untreated hypercalcemic renal insufficiency is lethal. The
other organ at risk is the brain. Psychologic disturbances may
develop into somnolence and finally coma. For all patients
with comas of questionable cause, a calcium-related coma
must be excluded.
When these symptoms of the hypercalcemic syndrome are
accompanied by additional symptoms that are characteristic of
a causal disease, the final diagnosis is facilitated. The so-called
organ manifestations of pHPT, such as renal stones, hyperpara-
thyroid bone disease, and recurrent peptic ulcers, may indicate
pHPT. Hyperthyroidism presents with its typical symptoms.
Hypercalcemia of malignancy must be considered in cases with
histories of, for example, previous breast cancer (for women)
or lung cancer or myeloma (for both men and women).
Diagnosis
The introduction of immunoassays for intact PTH-1– 84 was
a breakthrough in the diagnosis of hypercalcemic states. The
simultaneous occurrence of hypercalcemia and increased (or
nonsuppressed) PTH levels proves the parathyroid origin of the
hypercalcemia. The parathyroid glands are at least contribut-
ing, even if another cause may be involved. If intact PTH levels
are low and suppressed, parathyroid involvement is excluded
and other possibilities must then be investigated (Table 2). As
a rule, elevated PTH levels in hypercalcemia are caused by
pHPT. A variant is tertiary hyperparathyroidism after a history
J Am Soc Nephrol 12: S3–S9, 2001 Hypercalcemic Crisis S5

Table 1. Symptoms of the hypercalcemic syndrome, organ manifestations of pHPT, and typical indications for other causes
of hypercalcemiaa
Components of Hypercalcemic Syndrome
Pathognomonic
Organ Manifestation of Findings for Other
Organ Destabilization to
Disturbance Resulting Symptom or pHPT Hypercalcemic
Hypercalcemic Diseases
(Reversible) Complication Crisis

Kidney Hyposthenuria, Polyuria, polydipsia, Oliguria, anuria, Nephrolithiasis FHH: hypocalciuria

hypercalciuria, exsiccosis, muscle azotemia (recurrent),
sodium and weakness, arrhythmia nephrocalcinosis
potassium
loss 3
hypokalemia
Intestine Increased gastric Loss of appetite, nausea, Increase Peptic ulcer Hyperthyroidism:
acid secretion, vomiting, weight loss, (recurrent), weight loss
pancreatic constipation pancreatitis
enzyme (calcifying),
secretion, cholelithiasis
delayed
intestinal
transport
Central Endocrine Weakness, tiredness, Somnolence,
nervous psychologic loss of initiative, coma
system syndrome, depression, dizziness,
EEG changes loss of appetite
Musculature Increases in Muscle weakness, Increase Hypercortisolism:
level of weakened reflexes Cushing
neuromuscular myopathy
excitability
Cardiovascular ECG: shortened Arrhythmia Cardiac arrest Rare calcinosis Hyperthyroidism:
system QT time (hypertension) (avoid tachycardia,
digitalis) hypertension
(large amplitude)
Skeleton Osteoporosis, ostitis Malignancies: bone
fibrosa cystica metastases
generalisata (von
Recklinghausen)
Ankles Chondrocalcinosis
(pseudogout)
a
pHPT, primary hyperparathyroidism; FHH, familial hypocalciuric hypercalcemia; EKG, electrocardiogram; EEG,
electroencephalography.

of long-lasting renal insufficiency. Extremely rare is the para-
neoplastic production of true PTH (6). FHH is sometimes a
trap. The lack of true symptoms and organ manifestations must
be taken into consideration; the best diagnostic clue is the
calcium clearance/creatinine clearance ratio, which is ⬍0.01 in
FHH.
Most patients who present with nonparathyroidal hypercal-
cemia suffer from a malignant disease. In cases in which there
are no symptoms indicating pHPT, the search for a malignant
disease should be initiated early. Approximately one-half of
the patients have elevated blood levels of PTHrP. This finding
is observed in many cases of cancer of the lung, esophagus,
skin, kidney, pancreas, liver, colon, or ovary. Even hemoblas-
tosis may produce PTHrP. If PTHrP levels are low, other
osteolytic factors may be produced by the tumor. Calcitriol
levels are sometimes increased. Other cases demonstrate the
production of interleukin-1, -6, or -11, transforming growth
factor-␣ or -␤, interferon, or granulocyte/macrophage colony-
stimulating factor. We recommend only the measurement of
PTHrP; the measurements of the other factors are expensive
and not as reliable. The result is of no importance for the
treatment, which should be uniformly performed with
bisphosphonates.
The rare nonmalignant, non-parathyroid-related hypercalce-
mias generally provide some hints in the clinical findings.
Difficulties may arise in cases of iatrogenic hypercalcemia. If
S6 Journal of the American Society of Nephrology J Am Soc Nephrol 12: S3–S9, 2001

Table 2. Diseases leading to hypercalcemia and indications for diagnosisa

Category Condition Mechanism Indications for Diagnosis

PTH-induced, pHPT Increased intestinal Ca2⫹ Ca2⫹ 1, PTH 1

parathyroid
Tertiary
hyperparathyroidism
Lithium-induced (long-term
treatment)
Nonparathyroid
paraneoplastic Humoral hypercalcemia of
malignancy
mechanical Immobilization at
preexisting bone diseases,
e.g., multiple fractures (in
young patients),
osteoporosis, Paget’s
disease of bone, acute
intermittent porphyria
thyroidal Thyrotoxicosis
corticoadrenal Acute disease in
glucocorticoids, acute
Addison’s disease,
postoperatively in
Cushing’s disease
renal Acute renal insufficiency
Exsiccosis
FHH
Hard-water syndrome
calcitriol-induced Sarcoidosis
Tuberculosis, histoplasmosis Overproduction of calcitriol
(lepra)
viral AIDS
PTHrP-induced Infantile idiopathic
hypercalcemia
iatrogenic/induced by Vitamin D intoxication
medications
Vitamin A intoxication
Thiazides (in conditions
prone to hypercalcemia)
Tamoxifen in metastatic
breast cancer
Theophylline
Salicylic acid intoxication
a
PTH, parathyroid hormone; PTHrP, PTH-related peptide; IL, interleukin; TNF, tumor necrosis factor; TSH, thyroid-stimulating
hormone; ACE, angiotensin-converting enzyme.
absorption, renal Ca2⫹
absorption, osteolysis
Same
Same
Secretion of osteolytic factors Staging for malignancy, tumor
like PTHrP, IL-1, IL-6,
TNF, prostaglandins, and
calcitriol
Calcium release from the
skeleton attributable to
immobilization
Increase in bone turnover
Lack of a PTH antagonist
Decrease in calciuria
Decrease in calciuria
Decrease in calciuria
attributable to a calcium
sensor defect
Dialysis using too great a
calcium gradient
Overproduction of calcitriol
Osteolysis by viruses
(PTHrP 1?)
Calcium absorption 1,
osteolysis 1
Osteolysis
Calciuria 2
“Flare up” because of
paradoxical receptor
activation
? History
? History
History: long-lasting secondary
hyperparathyroidism, Ca2⫹ 1,
PTH 1
History: long-lasting lithium
treatment, Ca2⫹ 1, PTH 1
markers 1, PTHrP 1, calcitriol
1, PTH 2
History, x-rays, exclusion of pHPT
(PTH 2)
T3 1, T4 1, TSH suppression,
PTH 2
Glucocorticoid diagnostic tests,
history, PTH 2
History, renal function 2
History, renal function 2
Calciuria 2, phosphaturia normal,
PTH normal or 1, Ca2⫹
clearance/creatinine clearance,
⬍0.01
Control of dialysate
X-ray of lungs, ACE 1, calcitriol
1
X-ray of lungs, tuberculosis
diagnostic tests, serologic
findings, calcitriol 1
History, serologic findings
Age, exclusion of other causes,
PTH 2, PTHrP 1
History, calcidiol 1, PTH 2
History
History
History
J Am Soc Nephrol 12: S3–S9, 2001 Hypercalcemic Crisis S7

Table 3. Symptomatic treatment of hypercalcemiaa

Side Effects,
Type Measure/Substance Dosage Specific Indication Mode of Action Complications

Fast-acting
diuretic Drinking of fluids 2 to 3 liters/d Universal Increase in None
low in calcium calciuria
IV infusion of saline 4 to 6 (10) Universal Increase in Volume expansion,
liters/d calciuria (via hypokalemia,
natriuresis) hypomagnesemia
Furosemide 20 to 40 to 500 Universal in cases Increase in Hypomalemia,
mg/d of fluid retention diuresis and hypomagnesemia
calciuria
100 mg/hr 3 Same Direct stimulation Same
24 h of calciuria
antiresorptive Bisphosphonates
clodronate 300 mg iv in 6 Universal (in Inhibition of In cases of too fast
to 8 h for 2 to preference in osteolysis administration,
6 days HHM) renal insufficiency
400 to 3200 mg Same Same Rarely gastrointestinal
orally for complaints
days or weeks
pamidronate 15 to 90 mg iv Same Same Same, occasionally
in 4 to 6 h feverish reaction
ibandronate 2 to 6 mg iv in Same Same None
2h
Calcitonin 200 to 500 IU/d Universal (adjuvant Inhibition of Nausea, vomiting,
drug) osteolysis escape phenomenon
Mithramycin, mostly 25 ␮g/kg iv In preference in Inhibition of Thrombopenia,
replaced by daily for 3 to HHM, parathyroid osteolysis leukopenia, liver
bisphosphonates 4d carcinoma and kidney damage
extractive Hemodialysis Ca2⫹-free Hypercalcemic crisis Dialysis of Ca2⫹ Dialysis-related
dialysate and renal from the
insufficiency circulation
Slow-acting
anti-absorptive Diet low in Ca2⫹ ⬍100 mg Universal Decrease in Ca2⫹ None
and vitamin D Ca2⫹/d supply and
absorption
Prednisone 40 to 100 mg/d Vitamin D Decrease in Ca2⫹ Iatrogenic Cushing’s
intoxication, absorption, syndrome
sarcoidosis (rarely increase in
HHM) calciuria
a
HHM, humoral hypercalcemia of malignancy; iv, intravenous. Digitalis and hydrochlorothiazides are contraindicated during
hypercalcemia.

the patient does not reveal that he or she took, for example,
vitamin D (as in Münchausen’s syndrome), diagnosis may be
difficult (7). It is not too rare for hypercalcemia to be caused by
more than one disease (e.g., immobilization in osteopathies). In
cases of severe hypercalcemia in which PTH levels are only
mildly elevated, the possibility of a second diagnosis should be
considered. There have been frequent reports of the coinci-
dence of pHPT and sarcoidosis (8), thyrotoxicosis (9), and
other conditions.
In cases of compensated hypercalcemia without relevant
renal insufficiency, diagnoses can be made in a conventional
way. However, hypercalcemic crises require early treatment,
so that the life of the patient is not at risk.
Because hypercalcemic crises are predominantly parathyro-
toxic crises, pHPT must be proven or excluded. Proven pHPT
requires emergency surgery performed by an experienced sur-
geon. Surgeons who do not often perform parathyroid explo-
ration should refer their patients elsewhere.
The following diagnostic program is recommended: (1)
careful history and examination; (2) x-rays of the head, thorax,
vertebral column, pelvis, and long bones, to exclude osteolytic
lesions attributable to pHPT, metastases, myeloma, or lung
S8 Journal of the American Society of Nephrology
cancer; (3) ultrasound examination of the abdominal organs, to
exclude hepatic, pancreatic, renal, or gynecologic tumors (oc-
casionally, kidney stones or nephrocalcinosis indicates pHPT);
and (4) laboratory studies such as phosphate, potassium, cre-
atinine, urea, alkaline phosphatase, sedimentation rate, and
proteinuria measurements (hypercalcemia is known) and blood
smears. Fast PTH measurement is only occasionally available.
If all findings are generally normal and no tumor is found,
pHPT should be suspected. Ultrasound examination of the
neck region is recommended; it reveals a hypoechogenic nod-
ule, consistent with a parathyroid adenoma, in approximately
two-thirds of cases. Experienced surgeons are content with this
result, but inexperienced surgeons are not more satisfied after
computed tomographic and magnetic resonance imaging ex-
aminations, which cause further delay.
During this diagnostic procedure, the patient should be re-
ceiving symptomatic treatment (see below). The combination
of calcium lowering within 12 to 24 h and emergency diag-
nostic testing should permit surgical treatment of pHPT within
24 h.
Treatment
Except in cases of FHH, hypercalcemia is always a risk for
patients. The risk is present even in cases of so-called asymp-
tomatic pHPT. Observation of patients without surgery is per-
mitted (10); the guarantee of regular diuresis and the avoidance
of additional factors such as immobilization cannot always be
achieved. If patients are hypercalcemic, they must be warned
that regular drinking of fluids low in calcium represents a kind
of life insurance. Patients should know all symptoms of the
hypercalcemic syndrome and should ask their doctors for cal-
cium control in case of any such symptoms.
If hypercalcemia is relevant (⬎2.8 mM), fluid supply should
be defined. Patients should drink approximately 3 liters/d, to
produce a urinary volume of 2 to 2.5 liters. Diuresis in this
range requires the control of potassium (as well as calcium) in
the blood (Table 3).
When the calcium concentration increases above 3 mM,
often drinking is no longer sufficient. Nausea and even vom-
iting may begin; the intravenous infusion of saline solution is
the treatment of choice. Again, potassium substitution must be
considered.
Diuresis can be increased with furosemide. Lower doses
stimulate natriuresis, which is accompanied by calciuresis. A
direct calciuretic effect of furosemide should be expected at
high doses of 100 mg/h (11).
Especially in cases of humoral hypercalcemia of malig-
nancy, the administration of bisphosphonates should be con-
sidered early. Available preparations are clodronate, pamidr-
onate, and ibandronate. Table 3 documents the increase in
potency in this family of drugs. The advantage of the more-
potent bisphosphonates is the need for smaller amounts, which
means that the infusion time can be shortened. In cases with
normal renal function, ibandronate can even be administered as
a bolus; without time pressures, we prefer to perform infusions
in 1 to 2 h. We think that the highly potent bisphosphonates
limit the requirement for calcitonin, which may produce side
J Am Soc Nephrol 12: S3–S9, 2001
effects and which quickly becomes inactive because of the
escape phenomenon (12). Because of the availability of the
highly potent bisphosphonates, mithramycin (which was of
great utility in the pre-bisphosphonate period) is no longer
needed.
Hypercalcemias accompanying neoplasias are often chronic.
It is then recommended that the bisphosphonate treatment be
accompanied by a reduction in the dietary calcium supply.
Diets low in calcium and vitamin D are recommended.
Glucocorticoids exert a calcium-lowering effect by reducing
calcium absorption. They are indicated only for rare hypercal-
cemias such as intoxicosis with vitamin D or its analogs. The
treatment of some hemoblastoses, e.g., myeloma, also includes
glucocorticoids. They may then exert “cytostatic” effects as
well as antiabsorptive effects in the gut.
Hypercalcemic crisis requires a special accelerated strategy.
The first question to answer is the following: is diuresis pos-
sible and efficient? If yes, intravenous saline treatment, sup-
ported by furosemide, should be combined with a potent
bisphosphonate.
If diuresis is restricted and does not promise a relevant effect
within a few hours, hemodialysis is the treatment of choice. We
recommend that hemodialysis be performed in a unit with
sufficient expertise. The dialysis bath should be low in or free
of calcium, depending on the individual situation.
Contraindicated medications during hypercalcemia are dig-
italis and hydrochlorothiazides. Digitalis may produce cardiac
arrest if administered during hypercalcemia. Thiazides reduce
calciuria and thus contribute to the severity of hypercalcemia.
As mentioned, diagnostic testing should proceed in parallel
with the symptomatic calcium-lowering treatment. Hypercal-
cemic crisis is a situation that requires improvement within
hours.
Conclusions
Hypercalcemic crisis is a life-threatening condition that is
currently rather rare; however, it presents the risk that medical
action may be too slow. Most cases of hypercalcemic crisis are
attributable to decompensating pHPT. They require neck sur-
gery performed by an experienced endocrine surgeon.
Within 12 to 24 h, two problems must be solved. On one
hand, a short diagnostic program should lead to the exclusion
of neoplasias producing hypercalcemia. On the other hand,
those hours should also be used to lower serum calcium levels.
One method is forced diuresis combined with the use of highly
potent bisphosphonates; in cases of impaired renal function,
calcium-free hemodialysis is the treatment of choice. Hyper-
calcemic crisis should be treated in a unit with appropriate
expertise.
Acknowledgment
This work was presented at the 6th Colloquium Dresden, Intensive
Care Nephrology 2000, May 26 to 27, 2000.
J Am Soc Nephrol 12: S3–S9, 2001
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