What happens when we ingest too much Sodium Chloride (NaCl)?

Excessive Sodium Chloride Ingestion: Clinical Consequences and Management

Excessive sodium chloride intake causes hypernatremia, volume overload, hypertension, and in severe cases can lead to neurological dysfunction, seizures, coma, and death. 1

Primary Pathophysiological Consequences

Hypernatremia and Cellular Dehydration

• Excess NaCl consumption elevates serum sodium concentration, creating hyperosmolar conditions that draw water out of cells, causing cellular dehydration and central nervous system dysfunction. 2, 3
• Fatal hypernatremia from salt ingestion is rare but documented, with serum sodium levels reaching as high as 209 mEq/L causing irreversible neurological damage. 1
• At the cellular level, hyperosmolar sodium directly damages neurons by reducing glucose metabolism, depleting ATP levels, and causing cell death. 4

Volume Overload and Cardiovascular Complications

• Excessive sodium intake stimulates thirst and subsequent water consumption, leading to isotonic fluid gain and expansion of extracellular fluid volume. 5
• This volume expansion manifests as edema, ascites (in cirrhotic patients), and worsening hypertension. 5
• In patients with impaired sodium and water excretion (heart failure, cirrhosis, nephrotic syndrome, chronic kidney disease), administering excess sodium at typical maintenance rates risks dangerous volume overload. 5

Metabolic Acidosis

• High chloride loads from sodium chloride solutions cause hyperchloremic metabolic acidosis, particularly problematic in neonates and children. 5
• This acidosis can lead to neurological morbidities and growth faltering in premature infants. 5
• The mechanism involves excessive chloride intake disrupting acid-base balance when chloride concentration equals sodium concentration in normal saline. 5

Clinical Manifestations by Severity

Mild to Moderate (Sodium 145-160 mEq/L)

• Thirst, nausea, vomiting, weakness, headache, and mild neurocognitive deficits. 2
• Confusion and altered mental status as sodium rises. 2, 3

Severe (Sodium >160 mEq/L)

• Delirium, profound confusion, impaired consciousness, ataxia, and seizures. 2, 3
• Coma, brain herniation, and death in extreme cases. 2, 1
• Surprisingly small amounts of salt (70-90 grams) can cause fatal hypernatremia. 1

Special Population Vulnerabilities

Dialysis Patients

• Excessive sodium intake in hemodialysis patients aggravates thirst, interdialytic fluid gain, and hypertension, creating a vicious cycle. 5
• Higher dialysate sodium concentrations (140-155 mmol/L) used to facilitate ultrafiltration paradoxically worsen these problems. 5
• Dietary sodium restriction is essential for effective blood pressure and volume control in maintenance hemodialysis. 5

Cirrhotic Patients

• Hypertonic sodium chloride administration in decompensated cirrhosis improves serum sodium but dangerously enhances volume overload and worsens ascites and edema. 5
• Should only be used for severely symptomatic hyponatremia with life-threatening manifestations (cardiorespiratory distress, seizures, coma) or pre-transplant stabilization. 5
• Correction must not exceed 8 mmol/L per day to avoid central pontine myelinolysis. 5

Pediatric Patients

• Neonates, especially extremely low birth weight infants, are vulnerable to both hypernatremia and hyperchloremic acidosis from excessive sodium chloride. 5
• Chloride intake should be slightly lower than the sum of sodium and potassium intakes (Na + K - Cl = 1-2 mmol/kg/day) to prevent iatrogenic acidosis. 5
• Children with heart disease, liver disease, renal dysfunction, or on certain medications (desmopressin, carbamazepine, cyclophosphamide) are at particularly high risk. 5

Critical Management Principles

Correction Rate

• For chronic hypernatremia (>48 hours), sodium should not be reduced by more than 8-10 mmol/L per day to prevent osmotic demyelination syndrome. 6
• Acute hypernatremia (<24 hours) can be corrected more rapidly, but close laboratory monitoring is essential. 3, 6

Prognostic Factors

• Age and initial serum sodium concentration are the most important prognostic indicators for survival. 1
• Very young patients and those with lesser degrees of hypernatremia have better survival rates. 1
• The type of therapy or rate of correction did not influence survival as much as these baseline factors. 1

Prevention Strategies

• Advising water restriction without concurrent sodium restriction causes unnecessary suffering from thirst and is not prudent. 5
• Sodium restriction should be the primary intervention, with water intake naturally following. 5
• In parenteral nutrition, consider using sodium lactate or sodium acetate instead of sodium chloride to reduce chloride load and prevent acidosis. 5

Common Pitfalls to Avoid

• Never use salt or saline solutions as emetics—surprisingly small amounts can cause severe hypernatremia. 1
• Do not rapidly correct chronic hypernatremia, even when starting renal replacement therapy. 6
• Avoid isotonic saline at maintenance rates in patients with edematous states (heart failure, cirrhosis, nephrotic syndrome). 5
• Do not ignore the chloride component—equal concentrations of sodium and chloride in normal saline are non-physiological and problematic. 5