Case Study 1
A 12-year-old patient with chronic renal failure developed hypermagnesemia (serum magnesium 3.3 mg/dL) as a result of excess antacid ingestion.
Which of the following electrolyte abnormalities is NOT associated with hypermagnesemia? (Select all that apply)
- A.
Causes hyperphosphatemia
- B.
Causes hyperkalemia
- C.
Causes hypernatremia
- D.
Causes hypercalcemia
The correct answers are A and B
Comment: Magnesium helps with skeletal muscle contraction, helps the immune system, adenosine triphosphate (ATP) formation, and cellular growth. Magnesium regulates blood glucose levels and carbohydrate metabolism, and it has a direct relationship with calcium and potassium, not sodium. Magnesium helps with vitamin activation, not minerals.
Case Study 2
Which are the causes of hypermagnesemia in this patient? (Select all that apply)
- A.
Addison disease
- B.
Chronic kidney disease (GFR < 30 mL/min/1.73 m 2 )
- C.
Tumor lysis syndrome
- D.
Hyperthyroidism
The correct answers are A, B, and C
Comment: Hypermagnesemia is commonly caused by kidney failure or drug-induced such as magnesium-containing antacid or laxatives. Less common causes include tumor lysis syndrome, seizure disorders, and prolonged ischemia. Diagnosis is based on a blood level of magnesium greater than 1.1 mmol/L (2.6 mg/dL).
Case Study 3
What are the signs and symptoms of hypermagnesemia? (Select all that apply)
- A.
Hypertension
- B.
Tachycardia
- C.
Hyperreflexia
- D.
Skeletal muscle weakness
The correct answer is D
Comment: Patients with hypermagnesemia would manifest decreased or absent deep tendon reflexes, bradycardia, hypotension, cardiac arrhythmias, and skeletal muscle weakness.
Case Study 4
Which electrocardiogram findings are characteristic of hypermagnesemia? (Select all that apply)
- A.
Shortened PR interval
- B.
Prolonged PR interval
- C.
Widened QRS complex
- D.
Shortened QRS complex
The correct answers are B and C
Comment: Typically, electrocardiogram findings for hypermagnesemia patients include prolonged PR intervals and widened QRS complexes.
Case Study 5
Which of the following electrolyte abnormalities would you expect to see with hypermagnesemia? (Select all that apply)
- A.
Hyperkalemia
- B.
Hyponatremia
- C.
Hypophosphatemia
- D.
Hypercalcemia
The correct answers are A, C, and D
Comment: Magnesium also has an indirect relationship with phosphorus. If the magnesium is high, the phosphorous will be low. Magnesium has a direct relationship to potassium and calcium. If the magnesium is high, the potassium and calcium will both be high.
Case Study 6
How would you treat the elevated serum hypermagnesemia level in this patient? (Select all that apply)
- A.
Stop antacid medication
- B.
Administer a loop diuretic
- C.
Consider hemodialysis
- D.
Increased fluid intake
The correct answers are A, B, C, and D
Comment: It is important to discontinue medications that cause hypermagnesemia such as laxatives and antacids. It is important to administer a loop diuretic like furosemide that increases urinary magnesium excretion. Increasing fluid intake and limiting the intake of magnesium-rich foods such as green, leafy vegetables and avocados will also correct hypermagnesemia. Limiting fluid intake will not help with hypermagnesemia.
Hypermagnesemia is defined as a serum magnesium level greater than 2.6 mg/dL. Symptomatic hypermagnesemia is fairly uncommon. It occurs most commonly in patients with renal failure after ingestion of magnesium-containing drugs, such as antacids or purgatives. Hypermagnesemia may also occur in patients with hypothyroidism or Addison disease. Symptoms and signs include hyporeflexia, hypotension, respiratory depression, and cardiac arrest.
At serum magnesium concentrations of 6 to 12 mg/dL (2.5 to 5 mmol/L), the ECG shows prolongation of the PR interval, widening of the QRS complex, and increased T-wave amplitude. Deep tendon reflexes disappear as the serum magnesium concentration approaches 12 mg/dL (5.0 mmol/L); hypotension, respiratory depression, and narcosis develop with increasing hypermagnesemia. Cardiac arrest may occur when blood magnesium concentration is greater than 15 mg/dL (6.0 to 7.5 mmol/L).
Treatment of severe magnesium toxicity consists of circulatory and respiratory support and administration of 10% calcium gluconate 10 to 20 mL intravenously (IV). Calcium gluconate may reverse many of the magnesium-induced changes, including respiratory depression. Administration of IV furosemide can increase magnesium excretion when renal function is adequate; volume status should be maintained.
Hemodialysis may be valuable in severe hypermagnesemia because a relatively large fraction (about 70%) of blood magnesium is not protein bound and thus is removable with hemodialysis. When hemodynamic compromise occurs and hemodialysis is impractical, peritoneal dialysis is an option.
Case Study 7
A 19-year-old woman was diagnosed with severe preeclampsia and noted to have hyperreflexia on the exam. She was started on magnesium sulfate intravenously for seizure prevention. She was given an intravenous loading dose of magnesium (5.0 g) over 30 minutes, followed by a continuous infusion of 3 g/h. Four hours later she became confused, unable to urinate and her deep tendon reflexes were absent.
What would you do next? (Select all that apply)
- A.
Administer 0.9% saline
- B.
Give intravenous calcium gluconate
- C.
Discontinue magnesium sulfate
- D.
Give intravenous phenobarbital
The correct answers are A, B, and C
Comment: The patient is showing signs of magnesium toxicity. Magnesium infusion was stopped, and she was started on 0.9% normal saline at 125 mL/h and 1.0 g of calcium gluconate intravenously over 5 minutes. Serum magnesium level came back at 7.4 mg/dL and her electrocardiogram (ECG) was unremarkable.
Magnesium sulfate is the drug of choice for seizure prophylaxis in preeclampsia. Seizure prevention can be achieved by lowering magnesium doses without inducing magnesium toxicity.
Case Study 8
A 16-year-old man with a known history of end-stage kidney disease (ESKD) was brought to the emergency department due to lethargy, confusion, and blurred vision. He has been on hemodialysis (HD) for 5 years. His family reported that he has been using a variety of over-the-counter medications for severe constipation. A neurological exam was remarkable for absent deep tendon reflexes.
How would you manage this patient? (Select all that apply)
- A.
Acute hemodialysis
- B.
Continuous renal replacement therapy (CRRT)
- C.
Peritoneal dialysis
- D.
Administer intravenous normal saline and calcium gluconate
The correct answers are A and D
Comment: The patient with ESKD developed hypermagnesemia due to ingesting large doses of milk of magnesia (MOM). His serum magnesium level was 8.3 mg/dL. ECG showed no significant abnormalities. He was given 0.9% normal saline and 1.0 g of calcium gluconate. He was urgently dialyzed. After a 4-hour dialytic therapy, his serum magnesium fell to 4.8 mg/dL. He was instructed to avoid magnesium-containing laxatives and antacids.
Case Study 9
A 17-year-old female presented to the emergency department with altered mental status and progressive general weakness. She had a history of chronic constipation. Laboratory tests showed a magnesium level of 6.9 mEq/L. Bradycardia and hypotension developed later. Abdomen computed tomography showed hyper-dense magnesium oxide tablets retained in the colon. A magnesium-free laxative was used for gastrointestinal (GI) decontamination. Despite the use of high-dose inotropic and an elevated trigger for transcutaneous pacing, the cardiac performance improved minimally, and prolonged hypotension and decreased perfusion led to hypoxic encephalopathy.
How would you have treated this patient now?
- A.
Initiate peritoneal dialysis
- B.
Initiate hemodialysis
- C.
Administer intravenous furosemide
- D.
Administer intravenous normal saline
The correct answer is B
Comment : In this patient, the magnesium oxide tablets were retained in the GI tract without adequate decontamination resulting in continuous absorption and severe hypermagnesemia. A delay in starting hemodialysis following calcium infusion caused the poor outcome.
Case Study 10
A healthy 20-month-old girl presented to the emergency department with episodes of vomiting and a reduced level of consciousness. The neurological examination showed a symmetric decrease in muscle tone, and the deep tendon reflexes were decreased. On admission, her magnesium (Mg) level was 10.5 mg/dL after receiving magnesium oxide for 4 days because of constipation. She was immediately administered calcium gluconate infusion (3.9 mEq) followed by continuous infusion at a rate of 0.23 mEq/h). She was hydrated with 0.9% sodium chloride to maintain good urine output with furosemide administrating to increase the Mg excretion. The level of the serum Mg decreased to 2.4 mg/dL, enabling her to regain consciousness.
What additional therapeutic measure would you recommend now?
- A.
Initiate hemodialysis
- B.
Initiate peritoneal dialysis
- C.
Administer phenobarbital
- D.
Discontinue magnesium-oxide
The correct answer is D
Comment: Prompt administration of intravenous calcium infusion and administration of normal saline and loop diuretic corrected hypermagnesemia without the need for dialysis.
Case Study 11
A 17-year-old male with a known history of type 2 diabetes mellitus presented with fever, cough, shortness of breath, and dysuria. On examination, the patient was semi-conscious, drowsy, and arousable to vocal commands. His vital signs included blood pressure: 120/60 mmHg, pulse: 118 beats/min, temperature: 101°F, PO 2 of 72% in room air, and respiratory rate of 28 breaths/min. Laboratory investigations showed hypercalcemia (13.1 mg/dL), deranged liver functions, and high ammonia levels suggestive of hepatic encephalopathy. Parathyroid hormone levels were within the normal range. The patient was symptomatically managed with antibiotics, lactulose (15 mL), and antacids, and hypercalcemia was managed with calcitonin (100 IU) and aggressive hydration. Three days later, his serum magnesium levels and creatinine levels started to rise. His calculated eGFR was 30 mL/min/1.73 m 2 . Hypermagnesemia persisted despite aggressive treatment with intravenous calcium gluconate and hydration along with loop diuretics and the patient succumbed due to multiorgan dysfunction.
What is the MOST likely cause of hypermagnesemia in this patient?
- A.
Acute renal failure
- B.
Hypokalemia
- C.
Hypocalcemia
- D.
Hyponatremia
The correct answer is A
Comment: Hypermagnesemia though rarely seen and reported in clinical practice could possibly contribute to increased mortality in critically ill patients. The main reason for hypermagnesemia in critically ill patients is decreased renal function.
Case Study 12
An 18-year-old male patient diagnosed with acute appendicitis underwent appendectomy. On day 2 post-surgery he developed coagulopathy and hypotension secondary to sepsis. He was started on vasopressor support, which included noradrenaline and vasopressin. The patient had acute kidney injury with hyponatremia, hypocalcemia, and hypokalemia. Hemodialysis was initiated. Persistent hypermagnesemia (serum magnesium > 5.6 mg/dL) developed despite the above measures and the patient continued to deteriorate leading to death.
What is the MOST likely cause of death in this patient?
- A.
Hypermagnesemia
- B.
Hypokalemia
- C.
Hyponatremia
- D.
Hypocalcemia
The correct answer is A
Comment: Combination of acute renal failure, hyponatremia, hypokalemia along with persistent hypermagnesemia resulted in death.
Case Study 13
A 17-year-old female with a brain tumor underwent surgery. She developed hypotension, hyponatremia, hypokalemia, hypocalcemia, acute kidney injury, and encephalopathy 4 days post-surgery. Dialysis was initiated and electrolyte abnormalities were corrected. The patient developed severe hypermagnesemia (serum magnesium level 8.1 mg/dL), which did not resolve despite treatment with calcium infusion and vasopressin treatment, and died because of multiorgan failure.
What is the MOST likely cause of this patient’s hypermagnesemia?
- A.
Hypocalcemia
- B.
Hypotension
- C.
Acute kidney injury
- D.
Hypokalemia
The correct answer is C
Comment: This patient developed hypermagnesemia in presence of acute kidney disease. Hypermagnesemia persisted after correction of other electrolyte imbalances suggesting acute kidney injury as the underlying cause for hypermagnesemia.
The major etiological factors for hypermagnesemia are decreased renal excretion, increased magnesium intake, and compartment leak or shift. Hypermagnesemia between 7 and 12 mg/dL causes decreased reflexes, confusion, drowsiness, bladder paralysis, flushing, headache, and constipation. A slight reduction in blood pressure and blurred vision caused by diminished accommodation and convergence may manifest. For higher values (> 12.0 mg/dL) muscle paralysis, paralytic ileus, decreased breathing rate, and low blood pressure may occur. Electrocardiogram (ECG) changes included an increase in PR and QRS interval with sinus bradycardia, atrioventricular block, coma, and cardiac arrest (exceeding 15.0 mg/dL) may ensue.
Case Study 14
A 19-year-old woman who had been treated for pneumonia a week ago presented with confusion, fever, shortness of breath, and generalized weakness. She had a history of hypertension, which was controlled with amlodipine 10 mg daily and hydrochlorothiazide 12.5 mg daily. She was receiving magnesium-containing laxatives for a week prior to admission. Laboratory investigation showed serum sodium 135 mmol/L, potassium 4.6 mmol/L, chloride 95 mmol/L, bicarbonate 3 mmol/L, blood urea nitrogen 15 mg/dL, creatinine 0.6 mg/L, and estimated glomerular filtration rate (eGFR) 109 mL/min/1.3 m 2 . Serum magnesium level was 5.9 mg/dL, calcium 8.9 mg/dL, and phosphate 3.5 mg/dL. Electrocardiography (ECG) showed a sinus rhythm with a heart rate of 58 beats/min and left bundle branch block (PR, 200 ms; QT interval, 473 ms). Urinary ultrasonography showed normal renal parenchymal echogenicity and thickness. Computed tomography of the abdomen revealed that the rectum was filled with feces and fluid, which suggested the presence of ileus. Intravenous hydration with normal saline, intravenous calcium infusion, and broad-spectrum antibiotics was started. Gastrointestinal decontamination was performed. Twelve hours after the patient’s admission, the magnesium level was rechecked, with a result of 7.18 mmol/L. Because of the patient’s hemodynamic instability (blood pressure, 60/40 mmHg; heart rate, 60 beats/min) and oliguria, she was transferred to the intensive care unit and was started on vasopressor support with norepinephrine and dopamine, intravenous hydration, and furosemide infusion. Three days after the cessation of magnesium intake and supportive treatment, serum magnesium level decreased (2.16 mg/dL), the patient was weaned from vasopressors, urine output was restored with no need to perform hemodialysis, and the patient was discharged with a full recovery.
Which of the following conditions was responsible for the observed hypermagnesemia in this patient? (Select all that apply)
- A.
Excessive magnesium intake
- B.
Bowel disorders
- C.
Pneumonia
- D.
Hypertension
The correct answer is A
Comment: This patient developed severe hypermagnesemia after taking magnesium-containing laxatives without preexisting renal dysfunction and was treated successfully. This case suggests that severe hypermagnesemia can occur in the absence of preexisting renal dysfunction, especially in patients with bowel disorders.
Case Study 15
A 15-year-old girl was admitted with acute pyelonephritis. During her hospital stay, she received magnesium-containing laxatives for chronic constipation. She became confused and lethargic on the seventh day of medication, although inflammatory markers were decreasing. Her blood pressure was 85/44 mmHg and her pulse was 65 beats/min. The physical and neurological examinations were unremarkable. The serum magnesium level was elevated to 6.11 mg/dL and peaked at 7.04 mg/dL. Concurrent laboratory studies showed serum creatinine 0.89 mg/dL, blood urea nitrogen 44 mg/dL, and serum calcium 7.1 mg/dL. Results of arterial blood gas analysis in room air was pH, 7.52; PO 2 , 84.9 mmHg; PCO 2 , 42 mmHg; bicarbonate, 34.4 mmol/L; and base excess, 10.8 mmol/L). Serum lactate level was 1.6 mmol/L. An electrocardiogram (ECG) showed a sinus rhythm with a heart rate of 62 beats/min. Intravenous hydration with normal saline, loop diuretics, and intravenous calcium administration was promptly initiated. Blood pressure improved with intravenous hydration (110/67 mmHg), and urine output was 3 L/day. Subsequently, the serum magnesium level decreased and was 2.12 mg/dL after three days. The patient was diagnosed with irritable bowel syndrome, and her treatment was planned with dietary modification and other laxatives.
What additional therapeutic measure would you consider?
- A.
Initiate hemodialysis
- B.
Initiate peritoneal dialysis
- C.
Initiate continuous renal replacement therapy
- D.
None of the above
The correct answer is D
Comment: This patient developed severe hypermagnesemia after receiving magnesium-containing laxatives in the absence of renal dysfunction and was treated successfully without dialysis intervention.
Hypermagnesemia is an uncommon but serious clinical condition that can be fatal. Magnesium-containing products are widely used as antacids or laxatives. This patient demonstrates that excessive use of magnesium-containing laxatives can cause severe hypermagnesemia even in patients with normal renal function. Physicians should be aware of the effects of these medications in constipated patients.
Case Study 16
What caused severe hypermagnesemia? (Select all that apply)
- A.
Acute kidney injury
- B.
Excessive use of magnesium-containing laxatives
- C.
Hypokalemia
- D.
Hypocalcemia
The correct answers are A and B
Comment: Severe symptomatic hypermagnesemia may result from unsupervised use of magnesium-containing over-the-counter laxatives, which are often considered benign. In the setting of renal insufficiency, severe magnesium toxicity can develop especially in the elderly. The presentation can mimic various medical conditions such as sepsis or respiratory failure and hence the clinician should have a high degree of suspicion to order further testing to successfully diagnose this potentially life-threatening electrolyte disturbance. Once diagnosed, treatment with rapid supportive measures—intravenous calcium, fluids, loop diuretics, and urgent hemodialysis are highly effective in preventing significant morbidity and mortality.
Case Study 17
This 1.6 kg male patient was born at 29 weeks gestation to a 19-year-old Gravida 1, Para 0 mother. Pregnancy was complicated by preterm labor, tobacco use, and marijuana abuse. Two doses of betamethasone were administered before delivery. The infant was delivered by spontaneous vaginal delivery with Apgar scores of 9 at 1 and 5 minutes. Resuscitation consisted of bulb suction and bag-mask ventilation. The infant required 5 cm of nasal continuous positive airway pressure and was weaned to room air within 24 hours. Intravenous fluids were started at birth. On the second day of life, nasogastric feeding with breast milk was initiated, and intravenous fluids were changed to total parenteral nutrition (TPN). On the 10th day of life, while on nasogastric feedings of 120 mL/kg/day and TPN of 40 mL/kg/day, the infant was noted to have hypotonia, temperature instability, and lethargy. Blood was drawn for a complete blood count and blood culture, spinal tap and urine culture were collected, and intravenous antibiotics were started. Initial arterial blood gases were consistent with severe metabolic acidosis; the infant developed hypotension, bradycardia, and apnea. He was intubated and received multiple boluses of Ringer lactate with dopamine, dobutamine, and epinephrine infusions. Acidosis was corrected with bicarbonate without any improvement in hypotension and bradycardia. On admission, he had refractory bradycardia with a heart rate of 80 to 100 beats/min, systolic blood pressure of 42 to 48 mmHg by Doppler, serum creatinine of 0.9 mg/dL, ionized calcium of 1.6 mmol/L, and total calcium of 11.2 mg/dL. The patient received multiple doses of epinephrine through the endotracheal tube and intravenously and continued on intravenous infusions of epinephrine, dopamine, and dobutamine for hypotension. Serum magnesium was 7.4 mmol/L after the episode. Liver enzymes, serum osmolality, and urine osmolality were within normal limits. The infant was stabilized with mechanical ventilation. An electrocardiogram (ECG) was consistent with sinus bradycardia, a head ultrasound was negative for hemorrhage, and the initial electroencephalogram (EEG) was consistent with diffuse encephalopathy. Echocardiography revealed a patent foramen oval without any structural anomalies. Nerve conduction studies showed neuromuscular junction blockade. The infant was given an infusion of calcium, normal saline along with furosemide. The serum magnesium level was monitored closely along with serum electrolytes. The patient weaned quickly from the ventilator, as serum magnesium level returned to normal, and he was intubated to room air on the 15th day after admission. Nasogastric feeding was started on the seventh day after admission when serum magnesium level was within normal limits and repeat EEG and nerve conduction velocity was normal. The infant continued to do well, and he was discharged on the 53rd day of life with an adjusted gestational age of 36 weeks. On discharge, he weighed 2680 g, was on room air, and was taking feedings well.
What is the MOST likely cause of hypermagnesemia in this patient?
- A.
Excessive magnesium intake through TPN
- B.
Sepsis
- C.
Acute kidney injury
- D.
Hyperparathyroidism
The correct answer is A
Comment: Hypermagnesemia in newborns causes parasympathetic blockade, including cutaneous flushing, hypotension, prolonged QT-interval, delayed intraventricular conduction, respiratory depression, neuromuscular blockade, and coma and clinically mimics a central brainstem herniation syndrome. In this case, the infant received erroneously prepared total parenteral nutrition (TPN), which contained excess amounts of magnesium sulfate.
Unexplained sudden onset of apnea, refractory bradycardia, and refractory hypotension should raise suspicion of hypermagnesemia, which is reversible if identified and treated early. Iatrogenic hypermagnesemia has been reported from the administration of parenteral magnesium, excessive magnesium in dialysate solution, and multiple doses of cathartic therapy given in conjunction with charcoal. Early recognition and treatment of hypermagnesemia may prevent or minimize life-threatening events; however, the vast majority of mild hypermagnesemia patients may be missed. Hypotension, electrocardiographic changes, and evidence of sedation appear at serum magnesium concentrations of 3 to 8 mEq/L. The disappearance of deep tendon reflexes, respiratory depression, weakness, and coma are reported at magnesium levels of 5 to 15 mEq/L; cardiac arrest is reported at serum magnesium levels of 20 to 30 mEq/L.
Appropriate initial treatment of hypermagnesemia involves removal of exogenous magnesium source, and the use of intravenous calcium. The exact mechanism of action of calcium is not known, but it causes displacement of magnesium from the cell membrane, which results in transient reversal of symptoms of hypermagnesemia. Intravenous infusion of glucose and saline are also conservative treatment modalities, but renal dialysis, either peritoneal or hemodialysis is the treatment of choice in refractory hypermagnesemia.
References
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