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Case report
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Severe hypocalcemia and life-threatening ventricular
arrhytmias: case report and proposal of a diagnostic and
therapeutic algorithm
Emanuele Cecchi1
Francesco Grossi1
Matteo Rossi2
Cristina Giglioli1
Maria Laura De Feo2
1
Cardiac Step-Down Unit, Department of Heart and Vessels,
Careggi Hospital and University of Florence, Florence, Italy
2
Endocrinology Unit,Careggi Hospital and University
of Florence, Florence, Italy
An 87-year-old woman was admitted to our cardiac stepdown unit because of asthenia, nausea, emesis and oliguria.
She had an history of previous myocardial infarction complicated by ischemic stroke.
The electrocardiogram (EKG) showed sinus rhythm, pre-existing left bundle branch block (LBBB), and a frequent non-sustained ventricular tachycardia (VT) (Figures 1 and 2).
An echocardiogram showed an a-kinetic posterior wall and a
hypokinetic middle-basal lateral wall, with a mild reduction in
left ventricular ejection fraction, and a mild mitral regurgitation.
Blood examinations showed severe hypocalcemia (3.5
mg/dL; n.v. 8.2 – 10.7 mg/dL), ionized calcium levels of 2.69
mg/dL (n.v. 4.30 – 5.30 mg/dL), hyperfosforemia (9.0 mg/dL;
n.v 2.5 - 5 mg/dL) normal total proteins (6.1 g/dL n.v 6.0 –
8.6 g/dL) and serum creatinine values of 2.7 mg/dL.
An infusion with calcium gluconate (2 g in 250 mL saline solution at a rate of 10 ml/h) was immediately started and after
12 hours the serum calcium concentration was 5.8 mg/dL
(n.v. 8.2 – 10.7 mg/dL). An oral administration of 3 g per day
of calcium carbonate was then added and after other 24
hours calcium serum concentration resulted 6.8 mg/dL. An
EKG at 24 hours from the admission showed sinus rhythm,
pre-existing LBBB, some ectopic ventricular beats that gradually became less frequent as calcium concentration raised
above 6 mg/dL. An endocrinologic consult was acquired after
which the dosage of parathormone (PTH) and vitamin D3
were requested. The following exams showed mild increase
in serum PTH (8.4 pmol/L; n.v. 1.3 – 7.6 pmol/L), normal
magnesium concentration, 25-0H vitamin D deficiency (7.5
ng/mL; n.v. >20 ng/mL), phosphate was 9.4 mg/dL (n.v. 2.5 5 mg/dL). Thyroid function indices were normal. The endocrinologic diagnosis was “hypocalcemic crisis in a patient
with chronic kidney disease and severe vitamin D deficiency”. The patient fully recovered and was dismissed in a medical ward after few days; her EKG once the calcium levels
were partially corrected is reported in Figure 3.
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Address for correspondence:
Emanuele Cecchi, MD, PhD
Cardiac Step-Down Unit, Department of Heart and Vessels,
Careggi Hospital and University of Florence
Viale Morgagni 85
50134 Florence, Italy
Phone: +390557949577 - Fax +390557947617
E-mail: [email protected]
Case report
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longation and, when severe, can predispose to life-threatening ventricular arrhythmias (3). Acute hypocalcemia can result in severe symptoms that require rapid admission to hospital and prompt correction. In contrast, when hypocalcemia
develops slowly, patients can be surprisingly free of symptoms (4).
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Summary
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Hypocalcemia is frequent in the setting of endocrine disorders, bone diseases and renal failure. When hypocalcemia is severe it can predispose to life-threatening ventricular arrhythmias; in such cases a rapid admission to
hospital and a prompt correction of electrolyte imbalance are needed. We report the case of an old patient
suffering from renal failure that was admitted to our cardiac step-down unit because of severe hypocalcemia associated with ventricular arrhythmias. Hypocalcemia
was promptly treated and an endocrinologic consult was
requested for investigating the causes of this electrolyte
imbalance. Our experience suggests the creation of a
new synergy between cardiologists and endocrinologists that led us to build a simple and schematic algorithm for the diagnosis and treatment of hypocalcemia.
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KEY WORDS: hypocalcemia; ventricular arrhythmias; diagnostic algorhytm.
Introduction
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Electrolyte disorders can alter cardiac ionic currents kinetics
thus promoting pro-arrhythmic effects (1). In particular, calcium plays a pivotal role since it regulates for neural transmission, membrane stability, bone structure, blood coagulation
and intracellular signaling. Hypocalcemia is defined as total
serum calcium (Ca) concentration < 8.5 mg/dL in the presence of normal plasma protein concentrations or a serum
ionized Ca concentration < 4.7 mg/dL (2) and is frequent in
the setting of chronic renal dysfunction. Hypocalcemia can
result in both ST segment modification and QT interval proClinical Cases in Mineral and Bone Metabolism 2015; 12(3): 265-268
Protocol
This experience led us to draft a protocol regarding the optimal
diagnostic and therapeutic strategy in patients presenting with
severe hypocalcemia in a cardiology unit. This protocol was
designed together with our colleagues of the Endocrinology
Department and is composed of the following steps (Figure 4),
in agreement with data reported in literature (4, 5).
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Figure 1 - EKG at admission.
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Figure 2 - Allarm during continuous EKG monitoring.
Conclusion
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Severe electrolytes imbalances can trigger life-threatening
arrhythmias and patients admitted to hospital with these alterations are frequently monitored in Cardiac Care Units.
In particular, patients with coronary artery disease and previous myocardial infarction are more prone to develop ventricular arrhythmias, so that a close monitoring is crucial in the
first hours of electrolytes deficits correction.
However, whereas magnesium and potassium depletion can
be easily managed and seldom require an endocrinologic
consult, hypocalcemia requires a particular attention and a
different approach given the complex physiological mechanisms that regulates calcium metabolism. Altered vitamin D
metabolism, phosphate retention and skeletal resistance to
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the actions of PTH represent the main causes of hypocalcemia in patients with renal failure like the one we described
in our report.
Moreover, in old patients like the one here reported, physical
examination can be challenging and some of the typical
signs of hypocalcemia (i.e. Trousseau’s sign, Chvostek’s
sign) (4, 6) could be misinterpreted or difficult to assess.
Severe hypocalcemia is not very common in clinical practice
and finding the real cause can be troublesome. In patients
experiencing such severe electrolyte disorder a special attention must be paid to home medications possibly leading to
this condition. In the case of our patient suffering from
hypocalcemia, none of the drugs she was taking at home
was found to be correlated with such dramatic low levels of
calcium.
Clinical Cases in Mineral and Bone Metabolism 2015; 12(3): 265-268
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Figure 3 - EKG once the calcium level was partially corrected.
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Severe hypocalcemia and life-threatening ventricular arrhytmias: case report and proposal of a diagnostic and therapeutic algorithm
DIAGNOSTIC ALGORHYTHM
1. Vital signs, 12 lead EKG.
2. Presenting symptoms , medical history, physical examination
3. Laboratory exams (serum calcium, sodium, magnesium, phosphate, other electrolytes, total proteins, protein
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profile, creatinine, alkaline phosphatase)
4. Arterial blood gas (ABG) analysis
Measure blood concentrations of 25-OH vitamin D and parathyroid hormone (PTH)
6. Start a 24 hours urine calcium collection
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7. Ask for endocrinologic consult
THERAPEUTIC ALGORHYTHM
CHRONIC HYPOCALCEMIA
Start oral therapy with a mean daily dosage of 1,5 g
of calcium.
Start intravenous calcium gluconate; a central venous
Treatment depends on the underlying cause; start
catheter is preferable to avoid irritation of surrounding
additional therapies (i.e. vitamin D, calcitriol,
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ACUTE HYPOCALCEMIA
(usually total calcium <7.5 mg/dL or ionized calcium
<4 mg/dL). Patient symptomatic.
tissue. One or two 10 mL ampoules of 10% calcium
thiazide diuretics) after endocrinologic consult.
gluconate diluted in 50 to 100 mL 5% dextrose and
infused over 5 to 10 minutes. Treatment can be
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repeated but often it offers only temporary relief.
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Ten 10 mL ampoules of 10% calcium gluconate in 1000
mL of 5% dextrose or 0.9% saline may be given at 50
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mL/h.
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Oral calcium should be administered concurrently.
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An arterial line is placed for frequent measurement of
ionized calcium.
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Continuous EKG monitoring
Figure 4 - Protocol for patients presenting with severe hypocalcemia in cardiology unit (7, 8).
Clinical Cases in Mineral and Bone Metabolism 2015; 12(3): 265-268
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E. Cecchi et al.
References
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El-Sherif N, Turitto G. Electrolyte disorders and arrhythmogenesis. Cardiol J. 2011;18(3):233-45.
Liamis G, Milionis HJ, Elisaf M. A review of drug-induced hypocalcemia. J Bone Miner Metab. 2009;27(6):635-42.
Nijjer S, Ghosh AK, Dubrey SW. Hypocalcaemia, long QT interval and
atrial arrhythmias. BMJ Case Reports. 2010; doi:10.1136/bcr.08.
2009.2216.
Cooper MS, Gittoes NJ. Diagnosis and management of hypocalcaemia.
BMJ. 2008;336(7656): 1298–302.
Fong J, Khan A. Hypocalcemia, updates in diagnosis and management
for primary care. Can Fam Physician. 2012;58(2):158-62.
Urbano FL. Signs of hypocalcemia: Chvostek’s and Trousseau’s. Hosp
Physician. 2000;36:43-5.
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The aim of this report was to provide a tool for cardiologists
and internists approaching to patients with severe hypocalcemia and severe life threatening arrhytmias. In particular,
we tried to furnish an initial algorithm to distinguish between
mild and severe disorders and investigate the possible etiology of this condition which is of primary importance also for
early treatment. First line exams can be initially requested by
cardiologists and internists; an endocrinologic consult represents the following step to investigate more deeply the causes of such a life-threatening electrolyte imbalance and outline the proper diagnostic and therapeutic approach. Our experience suggests the creation of a new synergy between
cardiologists and endocrinologists.
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Clinical Cases in Mineral and Bone Metabolism 2015; 12(3): 265-268