Electrolyte Disturbances in Eating Disorders
Electrolytes & Eating Disorders
Eating disorders can cause a deficit in electrolytes — including potassium, sodium, magnesium and phosphorous — which play important roles in many of the key functions of the body and can become compromised with malnutrition, purging and/or dehydration. Electrolyte disturbances can lead to the development of a wide range of medical complications across the gastrointestinal, cardiovascular, musculoskeletal, renal (urinary) and nervous systems.
Common Electrolyte Abnormalities
Common electrolyte abnormalities include hypokalemia, hyponatremia, hypomagnesemia and hypophosphatemia.
Hypokalemia (Low Potassium)
Hypokalemia is the most common electrolyte abnormality, with one study finding 42.4% of patients with AN-BP, 26.2% of patients with BN and 14.2% of patients with AN-R to have hypokalemia in an inpatient/residential level of care. Hypokalemia more commonly develops by excessive loss of potassium through emesis (vomit), stool or urine without adequate replacement, although it can also happen during the refeeding process.
Potassium is the main intracellular electrolyte that maintains the resting membrane potential of the cells in the body (although it also has many other functions) which is especially important for muscle and nerve function. Signs of low potassium may include:
- Nausea and vomiting
- Heart palpitations or arrhythmias
- Muscle weakness, twitches, or cramps
- Tingling or numbness
- Rhabdomyolysis (muscle breakdown)
- Polyuria (excessive urination)
- Polydipsia (excessive thirst)
Correcting potassium depends on severity and whether or not metabolic alkalosis is present. Critically low levels of potassium (<2.5 mEg/L) generally require both intravenous and oral potassium, while higher levels (>2.5 mEg/L) in patients that are asymptomatic and have no ECG changes can usually be corrected more slowly with oral potassium supplementation. Dehydration and hypomagnesemia also need to be corrected.
Hyponatremia (Low Sodium)
Low serum sodium is the second most common electrolyte disturbance seen in eating disorder patients, with one study finding 17% of patients with AN-BP, 16% of patients with AN-R and 8.5% with BN experiencing hyponatremia at an inpatient/residential level of care.
Low sodium in eating disorders can be caused by several etiologies: hypovolemia (dehydration from either reduced fluid intake and/or purging), medications, and excessive water intake (primary polydipsia). Malnutrition is also associated with a reduced ability of the kidneys to excrete free water related to reduced solute intake.
Sodium is the main extracellular cation in the body, helping to maintain blood volume, cell volume and nerve and muscle function. Symptoms of hyponatremia can include:
- Nausea and vomiting
- Loss of energy, drowsiness or fatigue
- Muscle weakness, spasms or cramps
Correction of hyponatremia can be done through IV fluids, increased salt intake, pharmacologic intervention, and via improved nutritional status, although the chosen intervention depends on the etiology of the hyponatremia and the severity of the low sodium. Too aggressive of correction of hyponatremia can rarely lead to a condition called central pontine myelinolysis, which is associated with potentially irreversible neurologic complaints.
Hypernatremia (Elevated Sodium)
Patients with eating disorders are also prone to develop hypernatremia (high serum sodium). This develops for one of two reasons: reduced water intake (dehydration) or diabetes insipidus. During the refeeding process, patients with malnutrition seem to develop increased urine output, and in extreme cases wherein there is too excessive of fluid loss, this can manifest as diabetes insipidus. Both of these conditions are treated with increased fluid intake along with nutritional rehabilitation.
Hypomagnesemia (Low Magnesium)
Development of hypomagnesemia is overall poorly understood, with studies suggesting a wide range of reported incidences (16-60%). There are no studies that report the distribution of low magnesium across eating disorder types, however it can be caused by decreased oral intake, diarrhea or diuretic misuse. Alcohol abuse is another common cause for hypomagnesemia.
Hypomagnesemia can also develop during the refeeding process, with studies suggesting this occurs about four to five days into refeeding. The mechanism through which hypomagnesemia is caused by refeeding syndrome is unclear, but may possibly be caused by intracellular movement of magnesium during the refeeding process.
Magnesium is an intracellular cation, with the most abundant stores found in bone, which serves as a vital cofactor in most enzyme systems and is involved in potassium and calcium metabolism. It is important for muscle, nerve, and cardiac function, amongst others. It is also a cofactor in all bodily reactions using ATP (adenosine triphosphate), the energy compound in our body that is compiled largely of phosphorous.
Symptoms of hypomagnesemia may include:
- Ventricular arrhythmias and other cardiac conduction abnormalities
- Nystagmus (abnormal eye movements)
- Muscle spasms and cramps
- Fatigue or weakness
- Abnormal bodily movements
For symptomatic, severe hypomagnesemia (<1.2 mg/dL), IV replacement is generally recommended. For milder hypomagnesemia, oral repletion can generally be started at 400–800 mg twice daily.
Hypophosphatemia (Low Phosphorous)
Low serum phosphate is a significant factor in the development of refeeding syndrome, but can sometimes appear prior. 6% of patients with anorexia nervosa have hypophosphatemia on admission, a predictor of hypophosphatemia in refeeding. However, development of hypophosphatemia is most related to BMI nadir on admission, as a much greater frequency of patients develop hypophosphatemia upon nutritional rehabilitation. It develops during the refeeding process when the glucose load of the ingested food increases insulin release, subsequently increasing phosphorous uptake and leading to a deficit of extracellular phosphate.
Phosphorous plays a vital role in all intracellular processes and the structural integrity of cells. Hypophosphatemia can cause diaphragmatic muscle fatigue, respiratory failure, bursting of red blood cells as they circulate through the bloodstream (hemolysis), rhabdomyolysis (skeletal muscle injury), edema and seizures (i.e., refeeding syndrome).
Symptoms of hypophosphatemia may include:
- Musculoskeletal pain
- Ventricular arrhythmias
- Numbness or reflexive weakness
Failure to adequately treat hypophosphatemia can lead to refeeding syndrome. Treatment requires aggressive repletion with either IV or oral replacement, dependent on the severity of the hypophosphatemia.
Complications of Electrolyte Abnormalities
Electrolytes are essential minerals that are vital to regulating many key functions across most of the organ system. A disruption of potassium, sodium, phosphorous or magnesium can impact neurological, cardiac, muscle, gastrointestinal and renal function.
Low serum potassium can cause electrocardiogram changes, including QT interval prolongation. QT interval prolongation can put patients at risk for life-threatening arrhythmias, including sudden cardiac death. Hypophosphatemia can also impact the heart, causing systolic heart failure and arrhythmias.
Both hypokalemia and hypophosphatemia can result in rhabdomyolysis (death of muscle cells), a potentially life-threatening condition. Hypophosphatemia can also contribute to rhabdomyolysis. The disruption of skeletal muscle integrity leads to the breakdown of muscle tissue, releasing various proteins and electrolytes into the bloodstream and extracellular space, causing:
- Elevated creatine kinase
- Electrolyte imbalances
- Acute renal failure
- Compartment syndrome, a condition of tissue injury due to significant edema that compromises blood flow
Prolonged hypophosphatemia leads to osteopenia, osteoporosis, rickets, or osteomalacia due to decreased bone mineralization. Hypomagnesemia also likely contributes to low bone density.
Delayed Gastrointestinal Transit
Without adequate potassium, the smooth muscle of the intestines and colon become weak and unable to move stool, delaying gastrointestinal transit and resulting in:
- Paralytic ileus (inability of the intestines to contract normally)
- Abdominal distention
Chronic potassium depletion also produces significant adverse effects in the kidney, known as hypokalemic nephropathy. Hypokalemic nephropathy is estimated to affect between 15-20% of patients with anorexia nervosa. The cause of hypokalemic nephropathy is thought to be due to renal vasoconstriction, reduced medullary blood flow and impaired renal angiogenesis brought about by hypokalemia. This can progress to end stage renal disease requiring hemodialysis.
Refeeding syndrome is a potentially lethal complication comprised of the various clinical complications that develop due to a shift in fluids and electrolytes that occurs in significantly malnourished patients receiving artificial refeeding.
Refeeding syndrome is believed to occur due to a sudden shift from a catabolic state (“break down” pathways) to an anabolic state (“build up” pathways). During the catabolic phase, the body is breaking down different tissue for energy to compensate for lack of nutritional intake, and phosphorous, potassium and magnesium are being depleted without replenishment.
Once a patient begins refeeding and consumes carbohydrates (glucose), the body releases insulin in response. Glucose is then taken into the cells and stimulates anabolic pathways, and in the process phosphorous, potassium, magnesium and thiamin are taken into the cells as well and begin to be depleted. Counterintuitively this causes the use of micronutrients to begin outpacing replenishment, causing deficiencies in intracellular and extracellular electrolytes.
DaSilva JSV, Seres DS, Sabino K, et al. 2020. ASPEN consensus recommendations for refeeding syndrome. Nutrition in Clinical Practice 35:178-95.
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