1.4 - Hypomagnesemia & Hypermagnesemia Flashcards
What is hypomagnesemia?
- Decreased serum magnesium < 1.5 mg/dL (normal 1.5 – 2.5 mg/dL)
- Most of the body’s magnesium stores are intracellular, primarily within bones. In hospitalized patients, the incidence can be around 12% although it can rise to as high as 65% in ICU patients due to a multitude of comorbidities including poor nutrition, malnutrition, high dose diuretics and renal toxic antibiotics.
What are 8 common causes of hypomagnesemia?
In patients with low magnesium, the cause can be obtained by taking a thorough history
1. Renal losses
- Diuretics, especially loop diuretics and thiazides
- 20-45% incidence is seen in renal losses. If need be, a 24 hour urinary magnesium excretion can help distinguish between GI and renal losses. A daily excretion of more than 10-30 mg/24 hours in a person with normal renal function indicates renal magnesium wasting. On the flip side, if the excretion is less than 10 mg, the cause of hypomagnesemia can be attributed to GI losses.
2. Chronic alcohol use accounts for 30% incidence. The cause appears to be alcohol induced renal tubular dysfunction causing excessive urinary excretion. This appears to slowly correct itself after approximately 4 weeks cessation.
3. Renal drug toxicity can be caused by use of the following in patients with decreased GFR causing urinary magnesium wasting
- Aminoglycosides
- Amphotericin B
- Cisplatin
- Calcineurin inhibitors (Cyclosporin, tacrolmus)
- Digoxin
4. Gastrointestinal loss. Gastrointestinal secretions contain magnesium but if they are continuous and unregulated the result is severe hypomagnesemia.
- Persistent diarrhea or laxative use or abuse. There is a loss of magnesium from both upper and lower GI tracts but the magnesium contents of the lower tract are higher. Therefore you see a milder hypomagnesemia with vomiting.
- Malabsorption and inflammatory bowel disease
5. Poor magnesium intake, often due to;
- Alcohol abuse
- Protein and calorie deficient dietary intake leading to malnutrition
- Acute insulin therapy, as in DKA
6. Acute pancreatitis – same process as hypocalcemia (saponification)
7. Proton pump inhibitors – particularly with chronic use of omeprazole (longer than a year). The incidence varied in patients that take concomitant diuretics. The PPI impair the absorption of magnesium
8. Familiar renal magnesium wasting – this primary cause of magnesium wasting is rare. Gitelman and Bartter Syndrome and EAST syndromes fall into this category
What are the subjective and objective findings on physical exam of hypomagnesemia?
Clinical manifestations can be grouped into neuromuscular, cardiovascular, other electrolyte abnormalities.
- Subjective – patients complain of muscle weakness and neurological symptoms of tremors that can progress to seizures. This is due to neuromuscular hyperexcitability.
- Objective (physical findings) – Trousseau’s and Chvostek’s signs (described in hypocalcemia). You may also note generalized tremors and muscle spasms..
What diagnostic tests are used to diagnose hypomagnesemia?
- If the hypomagnesemia is severe, the calcium and potassium will also be decreased (check these)
- Urinary magnesium excretion less than 3 mEq/24 hr denotes a body deficiency
- Check an EKG – look for a prolonged QTc and/or both atrial and ventricular arrhythmias. There can be widening of the QRS, peaked T waves. The more severe the magnesium depletion, the higher the possibility of EKG changes.
How do you treat patients with hypomagnesemia?
Treat them based on symptoms:
Mild – moderate symptoms, non-emergent:
- 4Gms mag sulfate IV in 1 liter of D5W over 3-6 hours then 2-4 grams in D5W over the next 12-24 hours.
- Reach a mag level higher than low normal. (> 1.5), unless the patient is having or is prone to arrhythmias. Then your goal is a level of 2.0 mg/dL.
- Monitor levels post infusion. The frequency should be 6-12 hours depending on the patient’s clinical status.
Severe symptoms (including seizures and/or ventricular arrhythmias).
- Give 2 grams IV in 50 ml of D5W over 5-10 minutes. May be given IVP if patients has fatal arrhythmias.
- Torsade de Pointes is a possibility.
- Then start an infusion as above.
- Patient should remain on continuous cardiac monitoring if arrhythmias have been documented or if you feel it is indicated for patient safety.
On who and how would you initiate oral magnesium replacement?
- It is to replace mildly decreased magnesium or for those patients with chronic hypomagnesemia.
- Magnesium chloride (Mag-L-100), 2 tablets TID OR Magnesium Oxide (Mag-Ox 400) 400 mg PO BID OR Magnesium lactate (Magtab SR) 84 mg PO BID.
- Even if the magnesium is only mildly decreased in hospitalized patients, they may not be able to tolerate PO replacement. IV supplementation may be needed.
What considerations should be made in patients with a GFR <30mL/min when replacing magnesium?
- Proceed slowly even if the serum magnesium is greatly decreased.
- They are at a higher risk of developing Hypermagnesemia quickly
- Reduce the IV dose by 50% and monitor lab frequently to avoid overcorrecting.
What is hypermagnesemia?
Serum magnesium > 2.5 mg/dl. It is fairly uncommon in the absence of renal failure or magnesium administration. Clinical consequences are unusual at a level less than 4.0.
What are the 4 common causes of hypermagnesemia?
1. Decreased renal function
2. Ongoing magnesium intake in patients with renal insufficiency. Patients may not be aware that the follow OTC meds contain magnesium:
- Antacids including magnesium hydroxide (Maalox)
- Cathartics (especially common in the elderly population). These include magnesium sulfate (Epsom Salt), Magnesium hydroxide (Milk of magnesia), Magnesium citrate
3. Massive magnesium intake
- IV magnesium sulfate in eclampsia
- Oral Epsom salt
4. Mild insignificant elevations can occur in theophylline intoxication, DKA and tumor lysis syndrome
What are the subjective and objective findings on physical exam for Hypermagnesemia?
The symptoms can be divided into three main categories: neuromuscular, cardiovascular and hypocalcemia. The severity of the symptom depends on the degree of increased magnesium.
Subjective – The patient can exhibit findings of weakness that progress to paralysis with respiratory failure. Increased magnesium levels decrease impulse transmission across the neuromuscular junction. They may also experience lethargy, nausea, vomiting or difficulty swallowing. Neuromuscular toxicity is the most consistent complication observed in patients.
Objective (physical findings) – Hypotension, conduction and bradycardia (CV affects), decreased DTRs on exam, muscle weakness to flaccid paralysis if severe Hypermagnesemia (levels 8-10 mEqL). Low calcium may be seen on lab results.
What laboratory/diagnostic tests are used to diagnose hypermagnesemia?
- Serum magnesium higher than 2.2 mg/dl
- Assess the BUN and creatinine to see if they are elevated indicating renal insufficiency as a possible contributing factor to the etiology
- Check Calcium levels - Moderate Hypermagnesemia can inhibit the secretion of PTH leading to a reduction in calcium concentration
- Does the EKG show lengthening of the PR interval, widening of the QRS or possible complete heart block (CHB)?
How do you manage a patient with hypermagnesemia?
- In all cases of Hypermagnesemia, stop all PO and IV intake
- If the patient has EKG changes: 10% calcium gluconate 1-3 grams, Calcium chloride 500-1000 mg, Furosemide (Lasix) 40 mg IV plus ½ NS 50-100 cc/hr
- Hemodialysis for patients with EKG changes can be considered if the patient’s magnesium is > 4.0 meq/L
- Symptomatic Hypermagnesemia: Prompt supportive therapy is critical including mechanical ventilation for respiratory failure and/or a temporary pacemaker for severe bradycardia.
- In all cases, once the etiology has been determined, prevention and patient education is key
