bubble_chart Overview

Water and sodium are simultaneously deficient, but the water deficit is less than the sodium deficit. The serum sodium is below the normal range, and the extracellular fluid is in a hypotonic state. The body reduces the secretion of antidiuretic hormone, decreasing water reabsorption in the renal tubules and increasing urine output to raise the osmotic pressure of the extracellular fluid. However, the volume of extracellular fluid decreases even further. Interstitial fluid enters the bloodstream, which can partially compensate for blood volume but causes the reduction in interstitial fluid to exceed that in plasma. Faced with a significant decrease in circulating blood volume, the body will prioritize maintaining blood volume over osmotic pressure. The renin-angiotensin-aldosterone system is activated, reducing sodium excretion by the kidneys and increasing the reabsorption of Cl^- and water. As a result, the sodium chloride content in urine significantly decreases. The drop in blood volume also stimulates the posterior pituitary to increase antidiuretic hormone secretion, enhancing water reabsorption and leading to oliguria. If blood volume continues to decline and the aforementioned compensatory mechanisms can no longer sustain it, shock will occur. This type of shock caused by massive sodium loss is also known as hyponatremic shock.

bubble_chart Etiology

There are many causes of hypotonic dehydration. In surgical patients, a common reason is the loss of extracellular fluid followed by inadequate replenishment of water or insufficient salt intake, leading to a relative deficiency of sodium in the body compared to water loss. Common causes include: a. Persistent loss of gastrointestinal digestive fluids, such as diarrhea, vomiting, digestive tract fistulas, or intestinal obstruction, resulting in significant sodium loss along with digestive fluids; b. Large-scale fluid exudation from wounds, such as burns or extensive postoperative fluid leakage; c. Excessive excretion of water and sodium by the kidneys, such as long-term use of diuretics that inhibit sodium reabsorption in the renal tubules.

bubble_chart Pathogenesis

When the sodium concentration in extracellular fluid decreases, leading to a hypotonic state, the body first reduces the secretion of antidiuretic hormone to excrete water and increases the secretion of aldosterone to retain sodium. Meanwhile, interstitial fluid enters the bloodstream, partially compensating for blood volume and maintaining circulatory volume. If excessive salt loss persists or continues, water continues to be excreted in the urine, the osmotic pressure of extracellular fluid drops, and water shifts from the extracellular space into the cells. As a result, both blood volume and interstitial fluid significantly decrease, leading to hypovolemic shock. This type of shock caused by substantial sodium loss is also known as hyponatremic shock. At this stage, renal blood flow and filtration rate decrease, resulting in reduced or absent urine output.

bubble_chart Clinical Manifestations

Symptoms vary depending on the degree of sodium deficiency. Common symptoms include dizziness, blurred vision, weakness, rapid and thready pulse, and in severe cases, confusion, muscular rigidity, cramping pain, weakened tendon reflexes, and unconsciousness. Based on the severity of sodium deficiency, clinical hypoosmolar dehydration is classified into grade III:

1. Grade I sodium deficiency: Patients experience fatigue, dizziness, numbness in hands and feet, and mild thirst. Serum sodium is below 135mmol/L, and urinary sodium is reduced.

2. Grade II sodium deficiency: In addition to the above symptoms, patients often exhibit nausea, vomiting, rapid and thready pulse, unstable blood pressure, blurred vision, and reduced urine output. Serum sodium is below 130mmol/L.

3. Grade III sodium deficiency: Patients may experience confusion, weakened or absent tendon reflexes, stupor, or even unconsciousness. Shock often occurs. Serum sodium is below 120mmol/L.

bubble_chart Diagnosis

Based on the history of fluid loss and the above clinical manifestations, the diagnosis is generally not difficult. The following tests can be used to confirm the diagnosis. a. Urinary Na⁺ measurement often shows a significant decrease; b. Serum Na⁺ measurement below 135mmol/L indicates hyponatremia and can determine the degree of sodium deficiency; c. Plasma osmotic pressure is reduced; d. Red blood cell count, hemoglobin level, hematocrit, blood non-protein nitrogen, and urea are all increased, while urine specific gravity is below 1.010.

bubble_chart Treatment Measures

In addition to actively treating the disease cause, the first priority is to replenish blood volume. Given the characteristic of sodium deficiency exceeding water deficiency, saline solution or hypertonic saline should be administered intravenously to correct the hypotonic state of body fluids and restore blood volume.

1. **Grade I and Grade II Sodium Deficiency** The required fluid volume for replenishment should be estimated based on the clinical degree of sodium deficiency. For example, in a patient weighing 60 kg with a serum sodium level of 135 mmol/L, the estimated sodium chloride loss is 0.5 g per kg of body weight, totaling 30 g of sodium chloride. Typically, half of this amount (15 g) is replenished initially, along with the daily sodium requirement of 4.5 g, resulting in a total of 19.5 g. This can be achieved by intravenous infusion of approximately 2000 ml of 5% glucose saline. Additionally, the daily fluid requirement of 2000 ml should be provided, with further adjustments based on the degree of dehydration. The remaining half of the sodium can be replenished on the second day.

2. **Grade III Sodium Deficiency** For patients presenting with shock, blood volume should be replenished first to improve microcirculation and tissue perfusion. A larger volume of crystalloid solution is required, and 200–300 ml of 5% sodium chloride solution can be administered initially to rapidly correct hyponatremia, restore extracellular fluid volume and osmotic pressure, and facilitate the movement of water out of edematous cells. Further administration of hypertonic or isotonic saline can be continued based on the patient's condition.

The required sodium salt supplementation can generally be calculated using the following formula:

**Required sodium salt (mmol) = [Normal serum sodium (mmol/L) – Measured serum sodium (mmol/L)]**

**× Body weight (kg) × 0.6 (0.5 for females)**

For example, in a 50 kg female sexually transmitted disease patient with a measured serum sodium of 118, the required sodium salt supplementation = (142 - 118) × 50 × 0.5 = 600 mmol. Since 17 mmol Na+ = 1 g sodium salt, 600 mmol sodium is approximately 35 g of sodium chloride. On the first day, half of the required sodium salt (17.5 g) plus the daily requirement (4.5 g) should be administered, totaling 22 g. This can be achieved by infusing approximately 430 ml of 3% sodium chloride solution, followed by about 1000 ml of isotonic saline. Serum sodium levels should then be re-measured to guide further treatment.

3. **Sodium Deficiency with Acidosis** After replenishing blood volume and sodium salts, acidosis is often corrected due to the body's compensatory mechanisms, and alkaline drug therapy is usually unnecessary initially. If blood gas analysis indicates persistent acidosis, 100–200 ml of 1.25% sodium bicarbonate solution or 200 ml of balanced salt solution can be administered intravenously, with further supplementation determined based on the patient's condition. Potassium salts should be supplemented once urine output reaches 40 ml/h.