*Electrolytes in the ICU DOI: http://dx.doi.org/10.5772/intechopen.96957*

#### **Figure 1.**

*Diagnostic approach to hyponatremia, starting with osmolality.*

the fastest medication to obtain in an emergency. Typical dose of two ampules of hypertonic bicarbonate is equivalent to �200 ml of 3% saline [8]. See **Figure 2**.


$$\text{Maximum Urine Output} = \frac{\text{Dietary Solute Intake}}{\text{Urine Osmability}} \tag{1}$$

Normal diet contains 600-900 mosmol of solute/day and the minimum urine osmolality is 60 mosmol/kg therefore the maximum urine output (see Eq. 1) in a normal patient would be:

$$\text{Maximum Urine Output} = \frac{900}{60} = \textbf{15} \,\text{litres per day}$$

Therefore, in patients with primary polydipsia, they will overcome the maximum urine output while patients with reduced solute intake will have reduced maximum urine output.

3.Vaptans

*DOI: http://dx.doi.org/10.5772/intechopen.96957*

*Electrolytes in the ICU*

hypokalemia.

concentration

[8, 9].

**2.2 Hypernatremia**

*2.2.1 Introduction*

gain.

**141**

*2.2.2 Clinical presentation*

*2.1.5 Overcorrection of sodium*

• Risk factors for over-correction are cirrhosis, alcoholism, malnutrition and

• Administration of potassium will also increase plasma sodium because it enters the cells, increasing intracellular osmolality and causing water to move from the extracellular space into the intracellular space, thus raising plasma sodium

• In a patient whose sodium was corrected outside 24 hour parameters can be started on rescue strategy. Desmopressin can be given (dose: 2mcg IV/subQ every 6 hours) to reduce free water output. Concomitantly, free water should be given (D5W at 6 ml/kg infused over 2 hours with labs after every infusion to determine rate of lowering) with the goal to bring sodium back within suitable levels for the next 24 hours. Once the sodium goal is achieved, the D5W can be stopped but desmopressin can be continued to prevent overly rapid correction

• Osmotic Demyelination syndrome: This syndrome usually has a delayed presentation 2-6 days after over-correction. Symptoms are dysarthria, dysphagia, paresthesia, quadriparesis and seizures. These symptoms are irreversible. MRI brain will show demyelinating lesions however may not appear for atleast 4 weeks after disease onset. Earlier detection may be possible

• Hypernatremia is defined as >145 mEq/L (mmol/L). This is often seen in hospitalized patients and is associated with increased mortality in patients [10–12]. Hypernatremia represents a deficit of water in relation to the body's sodium stores which can result from a net water loss or a hypertonic sodium

• Most patients with hypernatremia are either very young or old [13]. Signs usually reflect central nervous system dysfunction. Elderly patients generally

• Brain shrinkage induced by hypernatremia can cause vascular rupture, with cerebral bleeding, subarachnoid and permanent neurological damage. This is counteracted by a solute movement to the brain which normalizes the brain

have few symptoms unless sodium exceeds 160 mEq/L [13, 14].

volume but does not correct hyperosmolality in the brain [15, 16].

• In patient with prolonged hyperosmolality, aggressive treatment with

hypotonic fluids may cause cerebral edema [17, 18].

with newer techniques such as DWI [8, 9].

**Figure 2.**

*Treatment algorithm for hyponatremia.*

	- 1.Treating the underlying cause
	- 2.Potassium Supplementation

3.Vaptans

