International Journal of Clinical Medicine, 2013, 4, 417-420 Published Online October 2013 (
Acute and Severe Hypercalcemia in a Near-Drowning
Tomoaki Takata1,2*, Akihisa Nakaoka1, Kazuhiro Kato1, Takeaki Fukui2, Satoko Maeta2,
Chishio Munemura2, Yoshikazu Murawaki2
1Department of Internal Medicine, Sanin Rosai Hospital, Yonago, Japan; 2Division of Medicine and Clinical Science, Tottori Univer-
sity School of Medicine, Yonago, Japan.
Email: *
Received August 14th, 2013; revised September 12th, 2013; accepted September 29th, 2013
Copyright © 2013 Tomoaki Takata et al. This is an open access article distributed under the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
An 80-year-old male was admitted to our hospital because of near-drowning in a hot spring. Besides hypoxia, serum
calcium was extremely high at 15.5 mg/dL on admission. After the treatment with normal saline infusion, furosemide
and calcitonin, the hypercalcemia was transient and didn’t recur during the course. The hot spring water contained much
calcium, so his hypercalcemia was considered to be a result of calcium absorption mainly through the alveoli. In this
case, we revealed that serum calcium rose within a short time after drowning, suggesting the necessity to measure the
calcium concentration of the drowning fluid in a near-drowning victim.
Keywords: Hypercalcemia; Drowning; Hot Spring
1. Introduction
Drowning is a life-threatening accident and care of hy-
poxia is the mainstay of therapy. The constitution of the
aspirated water has rarely been considered to be impor-
tant, except for the difference between sea-water and
fresh water. Electrolyte disability in near-drowning vic-
tim has been a rare complication and has been considered
to seldom need treatment. On the other hand, there are a
few cases of lethal hypercalcemia complicating a near-
drowning in unusual circumstances such as in the Dead
Sea [1]. We report a case of severe hypercalcemia com-
plicating a near-drowning in a hot spring.
2. Case Report
An 80-year-old male was admitted to our hospital. He
has a past history of hypertension and ventriculoperito-
neal shunt after subarachnoid hemorrhage. His regular
medications were famotidine, olmesartan, and amlodip-
ine. He was found drowning in a hot spring. He was
breathing by himself when rescued and transferred to our
hospital 22 minutes later.
When arriving, he was conscious but disoriented. His
body weight was 65 kg. His body temperature was
38.6˚C, the pulse rate was 122 beat per minute and regu-
lar, blood pressure was 206/110 mmHg, and his satura-
tion of oxygen was 88% while receiving 15 L/min oxy-
gen by reservoir mask. His skin was wet. Auscultation of
the chest revealed coarse crackles at both lungs. No neu-
rologic dysfunction was seen.
An electrocardiograph, chest radiograph, and blood
tests were performed at the emergency room. The elec-
trocardiograph revealed heart rate of 115 beat per minute
with multiple premature ventricular contraction and pre-
mature atrial contraction. The QT interval corrected for
heart rate was 0.404 second. The chest radiograph
showed bilateral congestion (Figure 1). Laboratory data
(Table 1) of the blood revealed white blood count of
9800/μL, neutrophil of 32.7%, hematocrit of 42.8%, he-
moglobin of 14.3 g/dL, platelet of 316 × 103/μL, sodium
of 137 mEq/L, potassium of 3.7 mEq/L, chloride of 104
mEq/L, calcium (Ca) of 15.5 mg/dL, phosphorus of 4.0
mg/dL, blood urea nitrogen of 15.5 mg/dL, creatinine (Cr)
of 0.95 mg/dL, total protein of 7.8 g/dL, albumin of 4.3
g/dL, asparate aminotransferase of 29 IU/L, alanine
aminotransferase of 15 IU/L, lactate dehydrogenase of
266 IU/L, creatine kinase of 138 IU/L, and blood glucose
of 150 mg/dL. Arterial blood gas analysis without re-
ceiving any oxygen revealed pH of 7.289, pCO2 of 55.0
mmHg, pO2 of 27.2 mmHg, 3 of 25.5 mmol/L,
BE of 1.6 mmol/L, ionized Ca of 3.94 mEq/L, and
*Corresponding autho
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Acute and Severe Hypercalcemia in a Near-Drowning Victim
Figure 1. Chest radiograph showed bilateral congestion.
Table 1. Laboratory findings on admission.
Complete blood count
WBC 9800 /μL
neu 32.7 %
RBC 473 × 104 /μL
Ht 42.8 %
Hb 14.3 g/dL
PLT 316 × 103 /μL
Blood chemistory
Na 137 mEq/L
K 3.7 mEq/L
Cl 104 mEq/L
Ca 15.5 mg/dL
P 4.0 mg/dL
BUN 15.5 mg/dL
Cr 0.95 mg/dL
TP 7.8 g/dL
Alb 4.3 g/dL
LDH 266 IU/L
CK 138 IU/L
Glucose 150 mg/dL
Arterial blood gas (room air)
pH 7.289
pCO2 55.0 mmHg
pO2 27.2 mmHg
HCO 25.5 mmol/L
BE 1.6 mmol/L
Ca2+ 3.94 mEq/L
Lactate 21.0 mg/dL
Tumor markers and endocrine studies (normal range)
intact PTH 12 pg/mL (10 - 65)
PTH-rP <1.0 pmol/L (<1.1)
1,25-(OH)2D3 32.1 pg/mL (20 - 60)
calcitonin 77 pg/mL (15 - 86)
ACE 5.1 U/L (8.3 - 21.4)
SCC 6.1 pg/mL
CYFRA 5.8 ng/mL (<3.5)
NSE 12.7 ng/mL (<10)
lactate of 21.0 mg/dL. Computed tomography (CT) of
head to abdomen revealed low density area at right cau-
date nucleus and pulmonary congestion at both lungs. No
tumor or lymphadenopathy was detected.
He was admitted to our intensive care unit. Arterial
blood gas analysis while receiving 15 L/min oxygen by
reservoir mask at 30 minutes after his arrival revealed pH
of 7.305, pCO2 of 51.7 mmHg, pO2 of 64.1 mmHg,
of 24.9 mmol/L, BE of 1.7 mmol/L, ionized Ca
of 4.36 mEq/L, lactate of 15.0 mg/dL. He was intubated
and mechanical ventilation with high PEEP was per-
formed for his respiratory failure, then nasogastric tube
was inserted and approximately 540 mL of fluid was
The serum Ca was extremely high, thus normal saline
injection was initiated and subsequently intravenous fu-
rosemide and intramuscular calcitonin 40 IU per 12
hours were administered. The ionized Ca level rose to
4.38 mEq/L after two hours of his admission. The second
hospital day, 12 hours after admission, the laboratory
data showed serum Ca of 13.2 mg/dL, magnesium of 1.6
mg/dL and Cr of 1.42 mg/dL. The third hospital day, 36
hours after admission, the laboratory data showed serum
Ca of 9.6 mg/dL and Cr of 1.55 mg/dL. Analysis of the
1470 mL of urine from up to 12 hours of his admission
revealed Ca of 13.7 mg/dL. His respiratory failure im-
proved and intratracheal tube was removed on the fifth
hospital day. The serum Cr was normalized at 0.65
mg/dL on the sixth hospital day. The hypercalcemia took
a transient course and did not recur (Figure 2). He was
well conscious and discharged on the fourteenth hospital
day without any complaints.
In order to evaluate the cause of the hypercalcemia,
additional examinations were performed. Laboratory data
on the second hospital day (also showed in Table) was as
follows; intact PTH of 12 pg/mL (normal range: 10 - 65),
PTHrP of <1.0 pmol/L (normal range: <1.1), 1,25-
(OH)2D3 of 32.1 pg/mL (normal range: 20 - 60), calci-
tonin of 77 pg/mL (normal range: 15 - 86), ACE of 5.1
U/L (normal range: 8.3 - 21.4), SCC of 6.1 mg/mL (nor-
mal range: <1.5), CYFRA 5.8 ng/mL (normal range:
<3.5) and NSE 12.7 ng/mL (normal range: <10). Some of
the serum tumor markers were elevated, however that
was considered to be a result of renal impairment. As the
renal function improved, the tumor marker decreased
within normal level on the tenth day. There were no evi-
dence of malignancy in chest CT, pharyngoscope and
Then we examined the characteristics of the hot spring.
The fluid contains much Ca of 240 mg/dL, which is very
high concentration, compared with that of fresh water
(1.5 mg/dL) and sea-water (58 mg/dL). It is considered
that the hypercalcemia was due to the absorption of Ca
contained in the fluid through the alveoli.
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Acute and Severe Hypercalcemia in a Near-Drowning Victim
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Hours after admission
Serum Ca
(mg/dL) Serum Cr
108 96847260483624 12 0
Figure 2. Clinical course of serum Ca and Cr. Unit conversion of Ca is as below; mg/dL = 4 × mEq/L.
3. Discussion
Near-drowning is a life-threatening accident and care for
hypoxia is the mainstay of its treatment [2]. When a
drowning patient can no longer hold the breath, some
amount of water is aspirated into the airways. As a reflex
response, coughing occurs and sometimes laryngospasm
occurs. Water in the alveoli causes surfactant dysfunction
and washout. This disrupts the integrity of the membrane,
increases its permeability, and exacerbates fluid, plasma,
and electrolyte shifts [3]. The combined effects of fluids
in the lungs, loss of surfactant, and increased permeabil-
ity of the alveolar-capillary membrane result in hypoxia.
It is well known that sea-water drowning and fresh
water drowning bring different clinical conditions. It has
only been emphasized the importance of discriminating
the two. Sea-water drowning causes hypernatremia and
dehydration. On the other hand, fresh water drowning
causes hyponatremia and hemolysis [4]. These electro-
lyte changes in near-drowning victim are seldom thought
to be a cause of death [2]. Hypercalcemia in near-drown-
ing victim is a rare complication except for a certain
situation [1,5,6].
The patient’s hypercalcemia had already appeared on
admission. It was characterized by acute onset, transient
course and no recurrence. In general, malignant tumor
and primary hyperparathyroidism were responsible for
almost of hypercalcemia [7], but there was no sign or
laboratory finding suggestive of these diseases. There
was no family history, medications or medical history
that could cause hypercalcemia. The hot spring water
contained 240 mg/dL of Ca, so his hypercalcemia was
probably due to absorption of Ca from aspirated fluid
through the alveoli. It was supposed that gastrointestinal
absorption of Ca played only a little part, because na-
sogastric tube was inserted soon after his admission and
amount of fluid was aspirated. Milk-alkali syndrome,
whose pathogenesis is excess intake of Ca, requires more
than 4 gram of Ca intake regularly [8,9].
Modell et al. demonstrated in experimental model that
change of sodium concentration occured within 5 minutes
after injection of fresh water in alveoli [10]. Another case
reports show that Ca absorption through alveoli precedes
that from gastrointestinal tract [1,5]. Analysis of the
urine during the first 12 hours revealed that urinary ex-
cretion of Ca was 2013 mg. That is equal to about 83 mL
of hot spring fluid. Oehmichen et al. reported that drown-
ing led to an aspiration of only 2 - 4 mL water/kg [11]. If
the same process occurred in the present case, total
amount of aspirated fluid was about 130 - 260 mL.
Hypercalcemia induces functional disturbances in
kidney, central nervous system, gastrointestinal tract and
cardiovascular system [8]. Severe hypercalcemia, defined
as serum Ca more than 14.0 mg/dL, often causes polyuria
and alters mental status. Arrhythmia is also the mani-
festation of hypercalcemia and lethal arrhythmia in a
near-drowning victim in the Dead Sea, in which Ca con-
centration is 1709 mmol/L, which have been reported [1].
Serum Ca level was the most predictable factor than
other electrolyte abnormalities in near-drowning in the
Dead Sea and Ca levels of more than 15.5 mg/dL were
significantly related to mortality [12]. Yagil et al. re-
ported that serum magnesium level was also important in
a near-drowning victim [1]. Although serum magnesium
level on admission was not measured in our case, it
seemed to be normal for the hot spring water containing
much less magnesium. In managing hypercalcemia, vol-
ume repletion and induction of saline diuresis followed
by loop diuretics are keys to therapy. Bisphosphonates
are often used to malignancy induced hypercalcemia, but
it takes 2 to 4 days to get its effect [13]. Calcitonin is an
effective adjuvant and has a rapid onset, but its effect is
Acute and Severe Hypercalcemia in a Near-Drowning Victim
transient and limited. It is difficult to know the exact
reason of renal impairment in the present case, but hy-
percalcemia could have affected the renal function. The
renal function improved as the serum Ca was normalized.
Here we report a case of acute and severe hypercalce-
mia in a near-drowning victim in hot spring due to the
excessive Ca absorption mainly through the alveoli.
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