Definition
- Dogs-serum magnesium >2.5 mg/dL
- Cats-serum magnesium >2.3 mg/dL
Pathophysiology
- Hypermagnesemia is less clinically significant than low total body magnesium in veterinary patients.
- Magnesium is second only to potassium as the most abundant intracellular cation; is found primarily in bone and muscle; is required for many metabolic functions.
- Serum magnesium is present in three forms: protein-bound form (approximately 25–30%) and chelated and ionized forms (together account for 70–75%).
- Magnesium absorption occurs primarily in the ileum. Absorption also occurs in the jejunum and colon.
- Magnesium is an important cofactor in the sodium-potassium ATPase pump that maintains electrical gradients across membranes.
- Interference with the electrical gradient can change resting membrane potentials; repolarization disturbances result in neuromuscular and cardiac abnormalities.
- The kidneys maintain magnesium balance with 10–15% reabsorbed in the proximal tubule, 60–70% in the thick ascending limb of the loop of Henle, and 10–15% reabsorbed in the distal convoluted tubule. Reabsorption within the distal convoluted tubule is under hormonal and neurohormonal control and determines the final urine concentration of magnesium.
- Any condition that severely lowers the glomerular filtration rate can elicit hypermagnesemia because magnesium homeostasis is largely controlled by renal elimination.
- High magnesium concentration impairs transmission of nerve impulses and decreases post-synaptic responses at the neuromuscular junction. When magnesium was given to anesthetized dogs at 0.12 mEq/kg/min, cardiovascular effects were not noted until plasma levels exceeded 12.2 mEq/L. The total dose of magnesium required to reach that level was 1–2 mEq/kg. It took cumulative doses of 5.9–10.9 mEq/kg to cause fatal cardiac arrhythmias (ventricular fibrillation).
- Magnesium has been called nature's calcium blocker; the most serious complications of hypermagnesemia result from calcium antagonism in the cardiac conduction system.
Systems Affected
- Cardiovascular
- Musculoskeletal
- Nervous
Incidence/Prevalence
Hypermagnesemia was found in 18% of hospitalized cats and 13% of hospitalized dogs. Most of these patients also had renal insufficiency or post-renal azotemia.
Geographic Distribution
N/A
Signalment
Species
Dog and cat
Breed Predilections
N/A
Signs
General Comments
- Usually caused by renal failure; clinical signs might be referable to azotemia and renal insufficiency. Clinical hypermagnesemia is reported most often in patients with preexisting renal disease that are oversupplemented with parenteral magnesium salts.
- Characterized by progressive loss of neuromuscular, respiratory, and cardiovascular function.
Historical and Physical Examination Findings
- Nausea, vomiting, weakness, bradycardia, flaccid paralysis, mental depression, and hyporeflexia.
- Hypotension and ECG changes, including delayed intraventricular conduction and prolonged QT interval, occur with increased serum magnesium.
- Atrioventricular block, respiratory depression, coma, and cardiac arrest have been observed in humans with serum magnesium concentrations >16 mg/dL.
Causes
- Renal failure.
- Intestinal hypomotility disorders and constipation.
- Endocrine disorders including hypoadrenocorticism, hypothyroidism, and hyperparathyroidism.
- Combined angiotensin-converting enzyme inhibitors and spironolactone administration.
- Excessive magnesium administration from magnesium-containing cathartic solutions given in conjunction with activated charcoal, magnesium-containing laxatives, and excess magnesium in peritoneal dialysis solutions.
- Iatrogenic oversupplementation in patients with concurrent renal disease.
Risk Factors
- Renal disease
- Intestinal hypomotility
- Massive hemolysis
- Hypoadrenocorticism
- Hyperparathyroidism
- Patients receiving angiotensin-converting enzyme inhibitors and spironolactone concurrently
- Excessive use of magnesium-containing cathartic solutions, especially in patients with renal insufficiency
