Milking the Diagnosis

Kenton Lane Dover, MD*, University of North Carolina, Chapel Hill, NC and Dr. John Stephens, MD, UNC School of Medicine, Chapel Hill, NC

Meeting: Hospital Medicine 2016, March 6-9, San Diego, Calif.

Abstract number: 496

Categories: Adult, Clinical Vignettes Abstracts

Case Presentation: A 67-year-old man presented with a 6-month history of severe episodic weakness. The episodes typically began with nausea and vomiting, followed by severe weakness involving inability to lift his upper or lower extremities against gravity or walk without assistance. Weakness typically lasted 12-24 hours before beginning to improve. He did not seek medical care for any of his previous episodes. During detailed medication history, the patient reported regular consumption of “a lot” of milk of magnesia for 3-4 years, up to 12 ounces in 24 to 48 hours. 

He had 1+ reflexes throughout and 4/5 strength in all extremities but was unable to maintain erect posture in a seated position. Cranial nerves were intact.

Serum magnesium was 12.2 mg/dL, creatinine 2.03 mg/dL (baseline 1.2) and calcium 7.7 mg/dL.

The patient was treated with intravenous normal saline as well as twice-daily intravenous furosemide.  His symptoms improved rapidly, with return to baseline strength, normalization of his deep tendon reflexes and ability to ambulate by hospital day 2, at which point he was discharged to home. 

Discussion: The general internist should be aware of the clinical manifestations of hypermagnesemia, which can have severe and even fatal complications. Plasma magnesium concentration is predominantly regulated by the kidneys via urinary excretion. Thus, symptomatic hypermagnesemia is most often seen in patients with renal impairment, though it can occur after large magnesium loads via intravenous, oral or colonic routes (Table 1).

Neuromuscular toxicity is the most common manifestation of hypermagnesemia, as it decreases transmission across the neuromuscular junction. Symptoms range from decreased or absent deep tendon reflexes to somnolence, paralysis and/or coma. Patients may find it difficult to maintain upright posture when sitting or standing. Bradycardia and hypotension can also be seen, with extremely elevated levels producing complete heart block and cardiac arrest. Common nonspecific symptoms include nausea, vomiting and flushing. Transient hypocalcemia often accompanies hypermagnesemia due to magnesium-related inhibition of PTH.

In the setting of normal renal function, treatment of hypermagnesemia involves cessation of magnesium containing therapies and may include loop diuretics to enhance magnesium excretion.

For patients with stage 3 to 5 chronic kidney disease (CKD), as well as in patients with mild to moderate acute kidney injury, initial management includes intravenous isotonic fluids along with a loop diuretic. Dialysis may be required in patients with advanced CKD, those with moderate to severe acute kidney injury, or in the setting of severe hypermagnesemia. Patients with severe manifestations or who require dialysis should initially receive intravenous calcium as a magnesium antagonist.

Conclusions: Given the potentially severe consequences of untreated hypermagnesemia, the general internist should be familiar with its manifestations and maintain a healthy index of suspicion in patients with weakness, especially in patients with renal insufficiency. Early recognition of hypermagnesemia in patients with signs and symptoms of neuromuscular toxicity is crucial for the initiation of appropriate therapies. Our case further demonstrates the importance of obtaining a detailed history from patients, including questions regarding use of over-the-counter medications.

To cite this abstract:

Dover KL, Stephens J. Milking the Diagnosis. Abstract published at Hospital Medicine 2016, March 6-9, San Diego, Calif. Abstract 496. Journal of Hospital Medicine. 2016; 11 (suppl 1). Accessed April 5, 2020.

« Back to Hospital Medicine 2016, March 6-9, San Diego, Calif.