Authors: Mahdieh Miri, Farhad Esmailsorkh, Ehsan Farhadi, Mitra Rahimi
Categories: Case Report, Magnesium sulfate overdose, Magnesium toxicity, Mg toxicity, Hemodialysis, Case report
Source: Journal of Medical Case Reports
Authors: Mahdieh Miri, Farhad Esmailsorkh, Ehsan Farhadi, Mitra Rahimi
Magnesium toxicity occurs mostly in patients with decreased renal function or in preeclamptic patients who underwent high-dose magnesium sulfate therapy. Iatrogenic injection of magnesium sulfate is a rare condition. Magnesium sulfate extensively influences heart, lung, and brain function. Therefore, it is crucial to manage magnesium sulfate overdose through intensive procedures if common treatments do not improve the patient’s prognosis. Our paper focuses on a case study of a patient who overdosed on magnesium sulfate and was managed through hemodialysis.
A 50-year-old Iranian woman was admitted to the hospital, following the injection of two vials of magnesium sulfate (25 g each) by emergency medicine services mistakenly, instead of the vial of glucose. At the entrance of the emergency ward, she became pulseless, and they initiated cardiopulmonary resuscitation and intubation. Electrocardiogram and laboratory results showed hypermagnesemia. Primary supportive interventions—fluid therapy and calcium gluconate injections—were ineffective in halting the progression of the patient’s symptoms. Therefore, we decided to initiate hemodialysis, which significantly improved the patient’s symptoms. Consequently, she improved and was discharged from the intensive care unit and the hospital.
Hypermagnesemia is a life-threatening and emergency condition that must be recognized and managed immediately. Hemodialysis should be considered promptly if basic supportive interventions such as calcium gluconate and fluid therapy are ineffective in treating hypermagnesemia.
Magnesium (Mg) is the fourth most abundant mineral in the body, and functions as a cofactor for enzymatic reactions [1–3]. The normal range of Mg concentrations in human serum is 1.8–2.3 mg/dl [4]. Mg sulfate is the drug of choice for the prevention, treatment, and management of recurrent seizures in patients with eclampsia and preeclampsia. It is also approved by the US Food and Drug Administration (FDA) for treating hypomagnesemia [5–7]. Given the increasing use of Mg in treating various conditions, further research is necessary to establish the safety of this therapy. Nonetheless, animal studies have examined the electrocardiographic (ECG) and electrophysiological effects of intravenous magnesium administration [8]. Despite limited case reports of hemodialysis for hypermagnesemia, we describe a patient with severe Mg sulfate toxicity who responded well to hemodialysis. The patient presented with multiple clinical symptoms, including loss of consciousness. Following treatment with hemodialysis, she experienced significant clinical improvement and was subsequently discharged from the hospital.
After a family struggle, a 50-year-old married Iranian woman was referred to Shahid Moddares Hospital in Saveh. Following the struggle, the patient became extremely agitated, and the emergency medical service (EMS) checked her vital signs, including blood sugar (BS), by fingerstick. Her BS was 65 mg/dL. Due to this low value, the EMS personnel mistakenly administered two vials of 50 mL of 50% magnesium sulfate (containing 25 g of magnesium sulfate in each vial) instead of a single vial of 50% dextrose. Immediately after the injection, the patient was flushed and lost consciousness; therefore, the EMS took her to the emergency ward of Shaheed Moddares Hospital. Upon arrival at the emergency department, the patient became pulseless before any assessment could be performed. The emergency physicians immediately initiated cardiopulmonary resuscitation (CPR) for 10 minutes, during which she was intubated. After restoring her pulse, they initiated supportive care and diagnostic procedures, including hydration, ECG, and laboratory tests. The patient’s companion mentioned no past medical history or kidney disease, and no drug or supplement for usual consumption. On examination, the skin was flushed; there was no sweating; the pupils were symmetric and dilated; the heart, lung, and intestinal sounds were normal; and the deep tendon reflexes (DTR) were hypoactive. Her blood pressure was 100/70 mmHg, and her pulse rate was 110 beats per minute.
The baseline renal function parameters were creatinine, 1.33 mg/dL; and estimated glomerular filtration rate (GFR), 49 mL/min/1.73 m^2^. The other initial laboratory findings were as blood glucose (BS), 484 mg/dL; serum sodium, 128 mEq/L; serum potassium, 2.2 mEq/L; calcium, 9.1 mg/dL; phosphorus, 3.2 mg/dL; magnesium, 4.9 mEq/L; urea, 38 mg/dL; aspartate transaminase (AST), 85 U/L; alanine transaminase (ALT), 107 U/L; lactate dehydrogenase (LDH), 528 U/L; troponin, negative on qualitative testing; and ceratine kinase-MB (CK-MB), 21 IU/L; venous blood gas analysis showed a pH of 7.14, PCO2 of 46.2 mmHg and bicarbonate (HCO3⁻) of 15.4 mEq/L.
Internal medicine and cardiology consultation were requested in the emergency ward, considering the laboratory results and ECG results, which revealed hypermagnesemia, hypokalemia, and hyponatremia. The ECG rhythm was irregular (160 bears per minute), the P wave was flatter, the ST depression in V2–V6, I, and II, and the ST elevation in aVR were obvious (Fig. 1).Fig. 1Electrocardiogram before hemodialysis
We considered acute coronary syndrome (ACS) as a potential cause of the ECG abnormalities, including ST changes. However, since the patient did not report any chest pain or dyspnea prior to her loss of consciousness and had no previous history of cardiac symptoms or risk factors for ACS, we suspected hypermagnesemia as the underlying etiology of the observed ECG alterations. Furthermore, the patient’s family history did not suggest any coronary artery issues. Considering the EMS personnel’s error in administering magnesium injection, our primary diagnosis was hypermagnesemia. Consequently, we promptly initiated appropriate treatment for hypermagnesemia without hesitation.
To achieve initial stabilization, we initiated supportive care with diuretics, intravenous isotonic fluids, and calcium gluconate. However, the patient did not respond to the treatment, and her Glasgow Coma scale (GCS) score remained at 4/15. Given the lack of progress, we decided against further delays and opted to treat her with hemodialysis. The decision to undergo hemodialysis was based on the Micromedex toxicology reference, which recommends hemodialysis for severe Mg toxicity. After 4 hours of hemodialysis, her serum Mg concentration was 3.1 mg/dL, her calcium concentration was 6 mg/dl, her phosphorus concentration was 0.6 mg/dl, and her consciousness improved, with a GCS score of 7/15. The patient’s condition significantly improved, as evidenced by clinical observations, laboratory tests, and ECG, after spending 24 hours in the intensive care unit (ICU) under intubated conditions. The next day, the patient was extubated and had a normal respiratory rate and O2 saturation (Fig. 2, Table 1). The patient remained in the ICU for 3 days, during which she clearly responded to treatment. After 48 hours of hospitalization, her serum magnesium level had normalized, reaching 2 mg/dL (normal range is 1.8–2.4 mg/dL).Fig. 2Patient stabilized and electrocardiogram became normal sinus rhythm, regular (100), normal P wave, normal QRS width, normal axis deviation, and no ST-elevation or depressionTable 1Laboratory resultsTime after admission/lab testUponarrival7 hours9 hours15 hours21 hours24 hours48 hours96 hoursPH7.147.217.347.367.42PCO2 (mmHg)46.254.335.242.633.2HCO3 (mmHg)15.421.218.723.522.5Blood sugar (mg/dl)484122111UREA (mg/dl)382183743Creatinine (mg/dl)1.331.041.010.870.93Magnesium (mg/dL)4.93.12.42.72.52Calcium (mg/dl)9.17.596.78.67.97.9Phosphorus (mg/dl)3.20.622.22.12.1Sodium (mEq/L)128137141142140142138Potassium (mEq/L)2.234.63.14.64.44White blood count (103/mm^3^)28.115.610.5Hemoglobin (g/dl)12.58.98.2Platelet (10^3^/mm^3^)166131110AST (SGOT) (U/L)85ALT (SGPT) (U/L)107Alkaline phosphatase (U/L)142Lactate dehydrogenase(U/L)526Creatine kinase(U/L)80CK-MB (U/L)28Troponin (qualitative)NegativeUric acid (mg/dl)6.7Timeline of clinical eventsCPR/intubation/calcium gluconate/HemodialysisEnd of hemodialysisICU administrationExtubation in ICUDischarge
The patient was intubated in the emergency department. Initial vital signs included a blood pressure of 100/70 mmHg, a pulse rate of 110 beats per minute, and oxygen saturation of 100%. In the ICU, her blood pressure improved to 120/70 mmHg, her pulse rate decreased to 90 beats per minute, and oxygen saturation remained at 100%. Following extubation, her vital signs blood pressure 110/70 mmHg, pulse rate 85 beats per minute, oxygen saturation 95%, and respiratory rate 12 breaths per minute. Prior to discharge, her vital signs were fully stabilized, with a blood pressure of 120/80 mmHg, pulse rate of 88 beats per minute, oxygen saturation of 96%, and respiratory rate of 13 breaths per minute.
Treatment was maintained with two vials of 10% calcium gluconate, administered three times daily, to correct hypocalcemia; 500 mg of phosphate Sandoz three times a day for hypophosphatemia; 5000 units of heparin twice a day; 40 mg of pantoprazole daily; and 2 L of 0.9% normal saline daily during her ICU admission. After 4 days, they discharged the patient in stable clinical condition with normal laboratory results. Before discharge, a comprehensive neurological examination was conducted, including assessment of consciousness, cognitive function, cranial nerve testing, and reflex testing. All findings were normal.
After discharge, we conducted follow-up with the patient over several weeks. The neurological examination and other clinical findings were unremarkable, and the blood Mg levels remained within the normal range.
As an anticonvulsant, Mg sulfate is frequently utilized to treat eclampsia and preeclampsia during pregnancy [9]. Mg sulfate extensively influences heart, lung, and brain function [10–12]. Predominantly, hypermagnesemia occurs when renal function decreases or when a large quantity of Mg is loaded [13, 14]. The clinical presentation of hypermagnesemia is associated with the serum Mg concentration. Nausea, vomiting, bradycardia, and hypotension occur at a Mg serum concentration of 4–7 mEq/L; moreover, loss of deep tendon reflexes and increased QT interval duration occur at a serum concentration of 8–10 mEq/L. Additionally, comatose, muscle paralysis, complete atrioventricular (AV) block, and cardiac arrest occur at serum levels greater than 12 mEq/L [15, 16].
The management of patients with hypermagnesemia is needed to eliminate Mg through renal excretion by high-volume normal saline infusion and loop diuretic consumption because of the specificity of loop diuretics, which inhibit tubular reabsorption of Mg in the thick ascending part of the loop of Henle. In patients with impaired renal function or exhibiting clinical symptoms of hypermagnesemia, hemodialysis should be considered as an appropriate management option. Calcium should be used to prevent the adverse neuromuscular and cardiovascular effects of hypermagnesemia in patients with symptoms of hypermagnesemia [17].
A large number of cases of hypermagnesemia have been reported in Japan due to Mg oxide (MgO) prescription as a laxative in elderly patients with constipation, most of whom had chronic kidney disease (CKD). In addition, some of the patients had dementia or cerebrovascular events and could not express their symptoms, and the Mg serum concentration was not measured in the initial assessment of the clinical presentation of patients as a routine laboratory test. They treated all of the patients with fluid infusion (normal saline) and diuretics, except for one patient who was treated with continuous hemodiafiltration (CHDF), although he died on hospital day 4 [18–22].
Akbar et al. reported 19 patients with Mg intoxication with severe preeclampsia among women treated with Mg sulfate, and this condition was significantly associated with prenatal death and low Apgar scores at 1 and 5 minutes. All patients with Mg intoxication were treated with calcium gluconate in accordance with the Indonesian national protocol. Three patients died; however, their deaths were not attributable to hypermagnesemia [23].
In 2021, a 34-year-old man was brought to the emergency department after being found unresponsive in a restaurant. An empty bottle of Mg supplements and ibuprofen were found beside him. Upon arrival, he was hypotensive and hypothermic, with a serum magnesium level of 11.7 mEq/L. He was admitted to the ICU, intubated, and treated with intravenous calcium gluconate, followed by continuous renal replacement therapy (CRRT), which reduced his serum magnesium levels. His hospital course was complicated by refractory shock requiring multiple vasopressors, abdominal compartment syndrome necessitating bedside laparotomy, aspiration pneumonia, acute respiratory distress syndrome (ARDS), and disseminated intravascular coagulation (DIC). Due to his deteriorating condition and poor prognosis, his family opted for comfort care. He died on hospital day 4 [24].
In a case reported by Cavell et al., a medication error involving the administration of 50 cc of magnesium sulfate instead of the intended 6 cc resulted in neurological manifestations due to hypermagnesemia. The patient was treated with calcium gluconate infusion, leading to clinical improvement within 6 hours [25]. Similarly, our study corroborates the efficacy of calcium gluconate in managing hypermagnesemia. However, in our case, approximately a couple of hours later, the patient exhibited resistance to conventional therapy, including calcium gluconate and isotonic fluid administration. Due to the lack of response, we opted for prompt escalation of treatment—hemodialysis—rather than relying solely on fluid therapy.
Our patient suffered an iatrogenic magnesium sulfate overdose, exacerbated by prehospital EMS administration. She underwent 4 hours of continuous hemodialysis, receiving concurrent calcium gluconate to mitigate cardiac complications. Post-dialysis, she recovered sufficiently for extubation. During her hospitalization, she developed hypocalcemia, hypophosphatemia, and hypokalemia, all of which were promptly corrected. Given the rarity of hemodialysis as a treatment for hypermagnesemia, its use in this case represented a critical clinical decision.
As highlighted in this report, hemodialysis is a rarely employed but critical intervention for severe hypermagnesemia. While magnesium toxicity is uncommon, it poses life-threatening risks, with clinical manifestations ranging from neuromuscular disturbances to altered mental status. In severe cases of hypermagnesemia, if the patient does not respond to calcium gluconate and diuretics, prompt hemodialysis can be highly effective and lifesaving.