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Magnesium: An Overlooked Electrolyte
The Journal of Emergency Medicine, Vol. -, No. -, pp. 1–3, 2017 Ó 2017 Elsevier Inc. All rights reserved. 0736-4679/$ - see front matter
http://dx.doi.org/10.1016/j.jemermed.2017.01.011
Clinical Communications: Adult MAGNESIUM: AN OVERLOOKED ELECTROLYTE Jaya Kala, MD and Ala Abudayyeh, MD UT Health Science Center at Houston-McGovern Medical School, Houston, Texas Reprint Address: Jaya Kala, MD, UT Health Science Center at Houston-McGovern Medical School, 6431 Fannin Street, MSB 5.134, Houston, TX 77030
, Abstract—Background: Hypermagnesemia is rare and usually iatrogenic. Due to decreased renal function, older patients are generally more susceptible to hypermagnesemia than are younger patients. Because it is not one of the commonly assessed electrolytes in the blood work panel of patients, high levels are usually missed. Case Report: An elderly gentleman with history of leukemia presented with complaints of shortness of breath and extreme weakness while walking. He was diagnosed with severe hypermagnesemia, but unfortunately succumbed to cardiorespiratory arrest. Why Should an Emergency Physician Be Aware of This?: Thorough history taking is crucial in evaluating weakness in elderly patients because the differential diagnosis is vast. Prompt consultation for emergent dialysis is critical to avoiding unfavorable outcomes due to electrolyte abnormalities. Ó 2017 Elsevier Inc. All rights reserved.
is unusual to be part of the commonly checked electrolytes when patients are admitted through the emergency department (ED). These are tested only when there is suspicion of elevated or decreased levels as per history and physical examination in the ED. We report a case of hypermagnesemia in an elderly patient with chronic kidney disease as a result of multiple laxative drug use for chronic constipation and multiple magnesiumcontaining enemas in the week before the ED visit. The patient unfortunately died from cardiopulmonary arrest despite initiation of dialysis. CASE REPORT An 80-year-old gentleman with history of chronic kidney disease, chronic obstructive pulmonary disease, and chronic myelomonocytic leukemia, was transferred from an outside hospital to our institution’s ED with complaints of shortness of breath, extreme muscle weakness, and continued hypoxia. An initial diagnosis of pulmonary embolism was made. He had complaints of fatigue, shortness of breath, and severe constipation for the last couple of days. He tried using milk of magnesia and several magnesium oxide tablets. He later went to a local irrigation clinic and underwent a total of five bowel regimens (contents of which were unknown) within a span of 2 days. However, he continued to have constipation and developed new limb weakness, slurred speech, and worsening shortness of breath, which prompted his current admission. On physical
, Keywords—hypermagnesemia; hypoxia; muscle weakness; dialysis
INTRODUCTION Magnesium is an important, yet often ignored, bivalent cation. It plays a vital role in membrane stability, muscle contraction, metabolism, and neuronal transmission (1). Hypermagnesemia is usually iatrogenic and is seen in those getting parenteral infusions for pre-eclampsia, eclampsia, and in those getting magnesium-containing cathartics for drug overdose or for bowel preparations before colonoscopies (1). Even though widely used, it
RECEIVED: 23 May 2016; FINAL SUBMISSION RECEIVED: 2 January 2017; ACCEPTED: 5 January 2017 1
2
examination, patient was obtunded, intubated on assist control mode of the ventilator, with a blood pressure of 89/52 mm Hg, heart rate of 50 beats/min, respiratory rate of 12 breaths/min, saturation was 96% while on FiO2 of 100%. He looked critically ill, with lungs that were clear to auscultation; S1, S2 heard but bradycardia appreciated, abdomen was soft, not distended, skin was moist and he had no leg edema. Initial blood work revealed acute kidney injury with a serum creatinine of 2.77 mg/dL (normal range 0.5–1.4 mg/dL) from his baseline serum creatinine of 1.8 mg/dL; blood urea nitrogen was 85 mg/dL (normal range 7–22 mg/dL), sodium 136 mEq/L (normal range 135–145 mEq/L), potassium 5.5 mEq/L (normal range 3.5–4.5 mEq/L), and calcium of 8.3 mg/dL (normal range 8.5–10.5 mg/dL). His arterial blood gas revealed that he had respiratory acidosis with partial pressure arterial CO2 (PaCO2) of 67 mm Hg (normal range 35–45 mm Hg); hypoxia with partial pressure arterial oxygen (PaO2) of 75 mm Hg (normal range 80–100 mm Hg), and O2 saturation of 93% while on
J. Kala and A. Abudayyeh
fraction of inspired oxygen (FiO2) of 100%. The patient was immediately transferred to the intensive care unit (ICU) for persistent hypoxia despite high-flow oxygen, initial bradycardia, new bundle branch block (Figure 1), and hypotension. Further laboratory work in the ICU revealed serum magnesium to be 13.8 mg/ dL (normal range 1.8–2.4 mg/dL). Nephrology was consulted for acute kidney injury and hypermagnesemia. Patient was started acutely on conventional hemodialysis and the serum magnesium was brought down from the initial 13.8 mg/dL to 4.8 mg/dL within 4 h. Due to the patient’s hemodynamic instability, he was started on high inotropic support with norepinephrine at 40 mg/ min and vasopressin at 0.04 U/min, was intubated, and was planned for transition to continuous renal replacement therapy. The patient, however, continued to be hypotensive, bradycardic, and later succumbed to sustained cardiopulmonary arrest, despite all resuscitative attempts as per the advanced cardiovascular life support protocol for bradycardia using atropine, epinephrine, and several cycles of chest compressions.
Figure 1. Electrocardiogram recording in the intensive care unit, showing the new bundle branch block.
Magnesium: An Overlooked Electrolyte
DISCUSSION Symptomatic hypermagnesemia can often occur as a result of excessive use of high magnesium-containing bowel regimens, as well as over-the-counter laxatives. Its effect is worse in the presence of kidney dysfunction. Clinical manifestations of hypermagnesemia are concentration-dependent (1). They range from mild nausea and vomiting to absence of deep tendon reflexes. At higher levels, paralysis of voluntary muscles can occur. This could result in respiratory compromise by affecting diaphragmatic muscles, as was illustrated in our patient. Higher levels cause conduction defects and hypotension (1). There is an increased risk of rebound hypermagnesemia in patients who are constipated due to the continuous absorption of nonexcreted magnesium-rich bowel preparations (2). This may have been the case in our patient, because even after conventional hemodialysis and successfully bringing down the magnesium level to <5 mg/dL, our patient continued to have conduction defects and hypotension. With this report, we want to bring attention to the need to broaden the differential diagnosis of hypoxia to include hypermagnesemia, especially in elderly patients with chronic constipation.
3
WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS? It is prudent to assess levels of all electrolytes during initial assessment of patients who come in with complaints of weakness and hypoxia. Early recognition and timely initiation of calcium infusions and hemodialysis could result in favorable outcomes in patients with hypermagnesemia (3). Timely referral to nephrologists is also important so that dialysis can be started in time to help with lowering the levels of these electrolytes and thereby lessen their deleterious effects. REFERENCES 1. Bertiger G, Jones E, Dahdal DN, Marshall DC, Joseph RE. Serum magnesium concentrations in patients receiving sodium picosulfate and magnesium citrate bowel preparation: an assessment of renal function and electrocardiographic conduction. Clin Exp Gastroenterol 2015;8:215–24. 2. Weng YM, Chen SY, Chen HC, Yu JH, Wang SH. Hypermagnesemia in a constipated female. J Emerg Med 2013;44:e57–60. 3. Khairi T, Amer S, Spitalewitz S, Alasadi L. Severe symptomatic hypermagnesemia associated with over-the-counter laxatives in a patient with renal failure and sigmoid volvulus. Case Rep Nephrol 2014;2014:560746.
http://dx.doi.org/10.1016/j.jemermed.2017.01.011
Clinical Communications: Adult MAGNESIUM: AN OVERLOOKED ELECTROLYTE Jaya Kala, MD and Ala Abudayyeh, MD UT Health Science Center at Houston-McGovern Medical School, Houston, Texas Reprint Address: Jaya Kala, MD, UT Health Science Center at Houston-McGovern Medical School, 6431 Fannin Street, MSB 5.134, Houston, TX 77030
, Abstract—Background: Hypermagnesemia is rare and usually iatrogenic. Due to decreased renal function, older patients are generally more susceptible to hypermagnesemia than are younger patients. Because it is not one of the commonly assessed electrolytes in the blood work panel of patients, high levels are usually missed. Case Report: An elderly gentleman with history of leukemia presented with complaints of shortness of breath and extreme weakness while walking. He was diagnosed with severe hypermagnesemia, but unfortunately succumbed to cardiorespiratory arrest. Why Should an Emergency Physician Be Aware of This?: Thorough history taking is crucial in evaluating weakness in elderly patients because the differential diagnosis is vast. Prompt consultation for emergent dialysis is critical to avoiding unfavorable outcomes due to electrolyte abnormalities. Ó 2017 Elsevier Inc. All rights reserved.
is unusual to be part of the commonly checked electrolytes when patients are admitted through the emergency department (ED). These are tested only when there is suspicion of elevated or decreased levels as per history and physical examination in the ED. We report a case of hypermagnesemia in an elderly patient with chronic kidney disease as a result of multiple laxative drug use for chronic constipation and multiple magnesiumcontaining enemas in the week before the ED visit. The patient unfortunately died from cardiopulmonary arrest despite initiation of dialysis. CASE REPORT An 80-year-old gentleman with history of chronic kidney disease, chronic obstructive pulmonary disease, and chronic myelomonocytic leukemia, was transferred from an outside hospital to our institution’s ED with complaints of shortness of breath, extreme muscle weakness, and continued hypoxia. An initial diagnosis of pulmonary embolism was made. He had complaints of fatigue, shortness of breath, and severe constipation for the last couple of days. He tried using milk of magnesia and several magnesium oxide tablets. He later went to a local irrigation clinic and underwent a total of five bowel regimens (contents of which were unknown) within a span of 2 days. However, he continued to have constipation and developed new limb weakness, slurred speech, and worsening shortness of breath, which prompted his current admission. On physical
, Keywords—hypermagnesemia; hypoxia; muscle weakness; dialysis
INTRODUCTION Magnesium is an important, yet often ignored, bivalent cation. It plays a vital role in membrane stability, muscle contraction, metabolism, and neuronal transmission (1). Hypermagnesemia is usually iatrogenic and is seen in those getting parenteral infusions for pre-eclampsia, eclampsia, and in those getting magnesium-containing cathartics for drug overdose or for bowel preparations before colonoscopies (1). Even though widely used, it
RECEIVED: 23 May 2016; FINAL SUBMISSION RECEIVED: 2 January 2017; ACCEPTED: 5 January 2017 1
2
examination, patient was obtunded, intubated on assist control mode of the ventilator, with a blood pressure of 89/52 mm Hg, heart rate of 50 beats/min, respiratory rate of 12 breaths/min, saturation was 96% while on FiO2 of 100%. He looked critically ill, with lungs that were clear to auscultation; S1, S2 heard but bradycardia appreciated, abdomen was soft, not distended, skin was moist and he had no leg edema. Initial blood work revealed acute kidney injury with a serum creatinine of 2.77 mg/dL (normal range 0.5–1.4 mg/dL) from his baseline serum creatinine of 1.8 mg/dL; blood urea nitrogen was 85 mg/dL (normal range 7–22 mg/dL), sodium 136 mEq/L (normal range 135–145 mEq/L), potassium 5.5 mEq/L (normal range 3.5–4.5 mEq/L), and calcium of 8.3 mg/dL (normal range 8.5–10.5 mg/dL). His arterial blood gas revealed that he had respiratory acidosis with partial pressure arterial CO2 (PaCO2) of 67 mm Hg (normal range 35–45 mm Hg); hypoxia with partial pressure arterial oxygen (PaO2) of 75 mm Hg (normal range 80–100 mm Hg), and O2 saturation of 93% while on
J. Kala and A. Abudayyeh
fraction of inspired oxygen (FiO2) of 100%. The patient was immediately transferred to the intensive care unit (ICU) for persistent hypoxia despite high-flow oxygen, initial bradycardia, new bundle branch block (Figure 1), and hypotension. Further laboratory work in the ICU revealed serum magnesium to be 13.8 mg/ dL (normal range 1.8–2.4 mg/dL). Nephrology was consulted for acute kidney injury and hypermagnesemia. Patient was started acutely on conventional hemodialysis and the serum magnesium was brought down from the initial 13.8 mg/dL to 4.8 mg/dL within 4 h. Due to the patient’s hemodynamic instability, he was started on high inotropic support with norepinephrine at 40 mg/ min and vasopressin at 0.04 U/min, was intubated, and was planned for transition to continuous renal replacement therapy. The patient, however, continued to be hypotensive, bradycardic, and later succumbed to sustained cardiopulmonary arrest, despite all resuscitative attempts as per the advanced cardiovascular life support protocol for bradycardia using atropine, epinephrine, and several cycles of chest compressions.
Figure 1. Electrocardiogram recording in the intensive care unit, showing the new bundle branch block.
Magnesium: An Overlooked Electrolyte
DISCUSSION Symptomatic hypermagnesemia can often occur as a result of excessive use of high magnesium-containing bowel regimens, as well as over-the-counter laxatives. Its effect is worse in the presence of kidney dysfunction. Clinical manifestations of hypermagnesemia are concentration-dependent (1). They range from mild nausea and vomiting to absence of deep tendon reflexes. At higher levels, paralysis of voluntary muscles can occur. This could result in respiratory compromise by affecting diaphragmatic muscles, as was illustrated in our patient. Higher levels cause conduction defects and hypotension (1). There is an increased risk of rebound hypermagnesemia in patients who are constipated due to the continuous absorption of nonexcreted magnesium-rich bowel preparations (2). This may have been the case in our patient, because even after conventional hemodialysis and successfully bringing down the magnesium level to <5 mg/dL, our patient continued to have conduction defects and hypotension. With this report, we want to bring attention to the need to broaden the differential diagnosis of hypoxia to include hypermagnesemia, especially in elderly patients with chronic constipation.
3
WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS? It is prudent to assess levels of all electrolytes during initial assessment of patients who come in with complaints of weakness and hypoxia. Early recognition and timely initiation of calcium infusions and hemodialysis could result in favorable outcomes in patients with hypermagnesemia (3). Timely referral to nephrologists is also important so that dialysis can be started in time to help with lowering the levels of these electrolytes and thereby lessen their deleterious effects. REFERENCES 1. Bertiger G, Jones E, Dahdal DN, Marshall DC, Joseph RE. Serum magnesium concentrations in patients receiving sodium picosulfate and magnesium citrate bowel preparation: an assessment of renal function and electrocardiographic conduction. Clin Exp Gastroenterol 2015;8:215–24. 2. Weng YM, Chen SY, Chen HC, Yu JH, Wang SH. Hypermagnesemia in a constipated female. J Emerg Med 2013;44:e57–60. 3. Khairi T, Amer S, Spitalewitz S, Alasadi L. Severe symptomatic hypermagnesemia associated with over-the-counter laxatives in a patient with renal failure and sigmoid volvulus. Case Rep Nephrol 2014;2014:560746.