|Year : 2018 | Volume
| Issue : 1 | Page : 12-14
Phosphate-induced hypocalcemia may have a role to play in a patient of recurrent cardiac arrest with severe hypophosphatemia
Mohammed Rizwan Jabbar, Arijit Sardar
Department of Anaesthesiology, Pain and Critical Care, All India Institute of Medical Sciences, New Delhi, India
|Date of Web Publication||10-Oct-2018|
Mohammed Rizwan Jabbar
Department of Anaesthesiology, Pain and Critical Care, 5th Floor, Teaching Block, All India Institute of Medical Sciences, Ansari Nagar, New Delhi - 110 029
Source of Support: None, Conflict of Interest: None
Hypophosphatemia is a common electrolyte abnormality in our day-to-day practice in Intensive Care Unit. Severe hypophosphatemia is usually multifactorial and can lead to devastating consequences such as cardiac arrest. Phosphate replacement can be considered in severe symptomatic hypophosphatemia. We describe a patient of chronic alcoholic and diabetic who presented with diabetic ketoacidosis, right-lung pneumonia, and septic shock. Subsequently, the patient developed recurrent cardiac arrest. Both hypophosphatemia and phosphate-induced hypocalcemia were attributed to be the cause of this recurrent cardiac arrest.
Keywords: Hypocalcemia, hypophosphatemia, recurrent cardiac arrest
|How to cite this article:|
Jabbar MR, Sardar A. Phosphate-induced hypocalcemia may have a role to play in a patient of recurrent cardiac arrest with severe hypophosphatemia. Saudi Crit Care J 2018;2:12-4
|How to cite this URL:|
Jabbar MR, Sardar A. Phosphate-induced hypocalcemia may have a role to play in a patient of recurrent cardiac arrest with severe hypophosphatemia. Saudi Crit Care J [serial online] 2018 [cited 2019 May 20];2:12-4. Available from: http://www.sccj-sa.org/text.asp?2018/2/1/12/243013
| Introduction|| |
Calcium and phosphate are essential minerals which play an important role in cell structure, cellular metabolism, acid–base homeostasis, and bone mineralization. Normal serum phosphate level is 2.5–4.5 mg/dl, and values <1 mg/dl is considered severe hypophosphatemia. Symptomatic hypocalcemia usually occurs at serum calcium level <2.5 mg/dl (equivalent to 0.635 mmol/L). Malignant ventricular arrhythmia and cardiac arrest are the most devastating cardiac complications of severe hypophosphatemia and hypocalcemia.,
| Case Report|| |
A 42-year-old male presented to the emergency department with history of fever, cough with expectoration, and shortness of breath for 1 week. He is chronic alcoholic and smoker for last 20 years. Before 3 years, he was diagnosed with diabetes mellitus. He was maintained on oral hypoglycemics which he stopped abruptly after 6 months and was lost to follow-up to the attending physician.
On admission, he had fever, tachycardia, hypotension, and tachypnea with 92% saturation on room air. Chest auscultation revealed decreased air entry and coarse crepitations on the right upper and middle zones. Routine investigations were ordered, and cultures were sent. A provisional diagnosis of diabetic ketoacidosis (DKA) with community-acquired pneumonia in septic shock was made based on blood gas analysis, urine and blood biochemistry, and chest X-ray. The patient was managed conservatively with fluid, insulin, and potassium. Broad-spectrum antibiotics were started empirically. Relevant laboratory investigations are listed on [Table 1].
The patient improved symptomatically on the 2nd day. He was started on enteral feed through nasogastric tube, slowly targeting to one-third of his daily calorie requirement along with intravenous fluid.
On the 3rd day morning, he developed symptomatic bradycardia followed by cardiac arrest. Cardiopulmonary resuscitation started, and adrenaline boluses were given at 5 min interval. The patient revived after 25 min of resuscitation. We introspected the reversible causes of cardiac arrest. Morning blood chemistry revealed hypophosphatemia of 0.3 mg/dl [Table 1] with normal sodium, potassium, and calcium. Severe hypophosphatemia was thought to be the cause of arrest. Potassium phosphate infusion was started at the rate of 0.6 mmol/kg ideal body weight over 4 h. Four hours later, the patient again developed cardiac arrest with ventricular tachycardia. Even after rigorous resuscitation with defibrillation, the patient could not be revived. Laboratory investigation at the time of second cardiac arrest revealed mild hypophosphatemia, hypocalcemia [Table 1], and normal potassium.
| Discussion|| |
Typical causes of hypophosphatemia in a critically ill patient include sepsis, DKA, refeeding syndrome, metabolic acidosis, trauma, medication, renal replacement therapy, etc. Even though the incidence of hypophosphatemia in the general population is rare, it is increased in certain subgroups of the patient. It is 2.2%–3.1% in the hospitalized patient, 65%–80% in sepsis, and 20%–40% in patients with DKA and alcoholism., Multiple factors might have contributed to the severe hypophosphatemia in our patient. Chronic alcoholism and malnutrition have predisposed the patient for baseline hypophosphatemia state. Intracellular phosphate shift because of insulin therapy for DKA and nasogastric feeding in the background of sepsis might have precipitated overt hypophosphatemia.
DKA is one of most common medical emergencies associated with depletion of phosphorous. Initiation of insulin therapy for DKA may precipitate hypophosphatemia within 6–12 h of therapy due to uptake of phosphate into insulin-sensitive cell and correction of metabolic acidosis. However, routine replacement of phosphate in DKA is controversial. However, parenteral therapy should be considered for patients with severe or symptomatic hypophosphatemia. Cardiac arrest of this patient was attributed to severe hypophosphatemia. The patient was also a chronic alcoholic and malnourished, hence refeeding syndrome might have contributed to the severity of hypophosphatemia. Body mass index <18.5 and alcohol abuse are two risk factors for the development of refeeding syndrome according to the National Institute for health and clinical excellence guidelines for identifying the patient at high risk of refeeding syndrome. Our patient had two bouts of cardiac arrest. First cardiac arrest is due to severe hypophosphatemia for which potassium phosphate was started. However, second cardiac arrest may not be mere consequence of hypophosphatemia. Overzealous phosphate infusion at a higher rate may have caused hypocalcemia, which might have contributed to second cardiac arrest. After the second cardiac arrest, serum-ionized calcium was 0.6 mmol/L. Symptoms of hypocalcemia start to appear with a calcium values <2.5 mg/dl (equivalent to 0.635 mmol/l). Phosphate infusion may cause the formation of calcium phosphate salts which precipitates when the solubility products are exceeded. Accidental infusion of potassium phosphate and sodium phosphate enema for bowel preparation, both have reported to cause cardiac arrest due to hypocalcemia. However, hypocalcemic arrest during resuscitation of hypophosphatemia is not reported in the literature to our best knowledge. Phosphate infusion is considered safe up to a total 45 mmol and 20 mmol/hr infusion without significant hypocalcemia and hypotension. Our patient received total 31.2 mmol of phosphate and an infusion rate of 7.8 mmol/hr which is much lower than the documented upper limit of safe dose. Probably lower baseline calcium level in our patient attributed to sepsis might have contributed much faster decrease in calcium level resulting hypocalcemic arrest.
| Conclusion|| |
We describe a chronic, alcoholic, and diabetic patient presented with DKA, right-lung pneumonia, and septic shock. The patient was stabilized and treated for DKA and sepsis. Nutrition initiated slowly on the second day with low-calorie feed. Insulin therapy and feeding have predisposed the patient to develop hypophosphatemia. Serum phosphate was measured daily which corroborated acute hypophosphatemia on third day resulting asystolic cardiac arrest. Phosphate infusion was started to correct hypophosphatemia. However, rapid overzealous correction of phosphate may have precipitated hypocalcemic cardiac arrest in a background of sepsis-induced hypocalcemic state. Basic understanding of calcium and phosphate physiology, tracking of decreasing trend of phosphate and calcium level, and infusing phosphate at much slower rate could have helped us to avoid such untimely demise.
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