Abnormal Electrolytes (Case 15)

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Abnormal Electrolytes (Case 15)

Rabeena Fazal MD and Alessandro Bellucci MD

Case: A 76-year-old woman with a history of hypertension and coronary artery disease presents to the ED with complaints of weakness, nausea, and muscle cramps. Her daughter states that she has been mildly confused over the past 2 days. She reports that her primary-care physician prescribed hydrochlorothiazide for elevated BP 2 weeks ago. The patient claims to be more thirsty than usual and, as a result, has been drinking more water. She denies any fevers, chills, vomiting, or diarrhea. Her other medications include metoprolol, aspirin, and simvastatin. On physical examination, the patient appears mildly lethargic and is oriented to name and place, but not to date. Her BP is 149/65 mm Hg without orthostatic changes, with a HR of 68 bpm. The cardiac and chest examinations are normal. No lower extremity edema is present. Neurologic examination reveals no focal deficits. Laboratory studies reveal a serum sodium 118 mEq/L, serum potassium 2.8 mEq/L, serum chloride 80 mEq/L, serum bicarbonate 29 mEq/L, BUN 34 mg/dL, serum creatinine 0.9 mg/dL, and serum calcium 11.2 mg/dL.

Differential Diagnosis








Speaking Intelligently

Electrolyte disorders are common clinical problems, especially among hospitalized patients. Fluids and electrolytes are normally very carefully maintained within narrow parameters to allow the cells of the body to function normally. Electrolyte abnormalities can affect the resting membrane potential, resulting in cardiac, neurologic, and musculoskeletal symptoms. Serum sodium concentration is a major determinant of extracellular osmolality, and abnormalities in sodium concentration lead to changes in intracranial pressure. The severity of the symptoms usually depends on how quickly the electrolyte disturbance occurs. The electrolytes that may be affected include sodium, potassium, and calcium. Since these disorders are accompanied by significant morbidity and mortality, appropriate diagnosis and treatment are essential.


Clinical Thinking

• Electrolyte disturbances represent an imbalance between ingestion and excretion, a shift between the intracellular and extracellular environment, or fluid loss or gain.

• Increased concentration of an electrolyte occurs as a result of excess total body amount, shift from intracellular to extracellular environment, or an absolute or relative water deficit.

• Decreased concentrations are a result of depleted total body amount, shift among compartments, or an absolute or relative water excess.


• For dysnatremias:

Search for causes of volume depletion, such as vomiting, diarrhea, GI bleeding, and decreased oral intake, or conditions associated with a low effective arterial blood volume, such as congestive heart failure (CHF), renal failure, and cirrhosis.

Review the patient’s medications and their side effect profile, as many medications can cause sodium disturbance. For example, thiazide diuretics can cause hyponatremia by interfering with the ability of the kidneys to dilute the urine.

Check the type of intravenous fluids being given in a hospital setting.

Assess whether the patient has neurologic symptoms related to hyponatremia, such as nausea, vomiting, headaches, mental status changes, or seizures. These symptoms are related to brain swelling and require immediate treatment.

• For potassium disorders:

Perform a careful review of the patient’s diet and medications.

Question the patient about GI disorders such as diarrhea or vomiting that can result in potassium losses.

Search for the presence of renal dysfunction, as this can result in an inability to excrete potassium.

Surreptitious vomiting or laxative abuse may be difficult to identify but should be excluded.

The family history is important, because there can be rare cases of hereditary potassium disorders.

• For calcium disorders:

Ask about water intake and urinary habits.

Polyuria and polydipsia are common in patients with hypercalcemia and hypokalemia, as these disturbances interfere with the action of ADH in the distal tubule, resulting in nephrogenic diabetes insipidus.

Ask about a history of renal disease, because hypocalcemia and hyperphosphatemia are common in patients with advanced renal dysfunction and secondary hyperparathyroidism.

Hypercalcemia incidentally found on an outpatient basis is most commonly related to primary hyperparathyroidism, and affected individuals may give a history of nephrolithiasis.

Malignancy can cause hypercalcemia; when it is the cause, the underlying malignancy is usually readily apparent.

Physical Examination

• Focus on signs of volume depletion or volume overload.

• Evaluate for mental status changes and other neurologic findings.

• The presence of Trousseau or Chvostek sign can point to a diagnosis of hypocalcemia.

Tests for Consideration

The diagnosis and treatment of fluid and electrolyte disorders are based on serum electrolyte concentrations, urine electrolyte concentrations, and serum and urine osmolality. Once the specific electrolyte abnormality has been diagnosed, additional tests can be done to aid in determining the etiology.

TSH and cortisol levels can exclude hypothyroidism and adrenal insufficiency, respectively, as causes of hyponatremia.

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• In potassium disorders, determination of acid-base status can aid in the workup.


Radiologic tests (e.g., chest radiograph, CT scan of the chest, neuroimaging) can provide evidence of malignancy, which can be a cause of hyponatremia or hypercalcemia.

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Hyponatremia is defined as a serum sodium concentration < 135 mEq/L. Hyponatremia may be hypertonic, hypotonic, or isotonic, associated with a high, low, or normal serum osmolality, respectively. Isotonic hyponatremia is the result of laboratory artifact due to a decreased aqueous component of plasma such as may be seen in patients with hyperlipidemia and hyperproteinemia. Hypertonic hyponatremia results from the presence of solutes, such as mannitol and glucose, which do not freely cross cell membranes, and represents a hyperosmolar state. Most hyponatremia is hypotonic, representing an excess of total-body water relative to total-body sodium, and is caused by impaired renal water excretion combined with continued water intake. Reasons for impaired water excretion include renal failure, volume depletion, high-ADH states, hypothyroidism, adrenal insufficiency, and low osmolar intake. Thiazides impair the ability of the kidneys to excrete free water, and, if the patient maintains a high water intake, as in the case illustrated above, a positive water balance ensues and hyponatremia results.


The symptoms of hyponatremia reflect cerebral edema and range from headache, nausea, vomiting, and mental status changes to seizures, coma, brainstem herniation, and death. The majority of patients present with mild symptoms such as nausea, weakness, and confusion. On exam they may have signs of hypovolemia, hypervolemia, or euvolemia.


Most patients with hyponatremia will have a low serum osmolality and a urine osmolality > 100 mOsm/kg, reflecting an impaired renal diluting ability (the normal renal response should be to dilute the urine to 60 mOsm/kg). The urine sodium concentration will vary depending on the source of volume loss (renal or nonrenal) and the amount of sodium intake.