Core pharmacology

Class Group

Crystalloid

Legacy Cicm Level

Level 1

Introduction

Hypertonic Crystalloid

PROS & CONS – See BELOW

Indications Uses

1. Treatment of severe, symptomatic hyponatraemia
2. Management of raised ICP
3. In nebulized form as an expectorant

Presentation

3%, 5% and 23.4%
Should be administered through CVC due to thrombophlebitis

Mechanism of action

Increased serum sodium concentration. Leads to increase in serum tonicity, leading to diffusion of intracellular fluid into the intravascular space, decreasing cerebral oedema.

Physiological effects

CNS: Decreased cerebral oedema, decreased ICP, may cause central pontine myelinolysis

CVS: Fluid shift into intravascular compartment increases plasma volume and may improve preload
? increase cardiac output
? increase BP

Adverse Effects Toxicity

1. Central pontine myelinolysis
2. Hypernatraemia and hyperosmolarity
3. NAGMA
4. Thrombophlebitis
5. Seizures

Absorption

IV.

Metabolism

Unmetabolized

Excretion

renally excreted

Special Points

Osm 900

Na 450
Cl 450

ADVANTAGES:
Cheap
• Stable in storage
• Easy to transport (small volume)
• Very rapid effect (peak @ 10 min, lasts 1
hour)
• Seems to have some sort of intrinsic antiinflammatory effect (may decrease MODS)
• May also have some rheological benefits
At least as potent as mannitol when it
comes to reducing intracranial pressure
• Less potential for hypovolemia than with
mannitol- the diuretic effect is less potent
• rapid restoration of intravascular volume,
BP and decreases ICP
• May have a better effect on cerebral blood
flow for a given reduction in ICP.
• Safe endpoint (serum sodium around 145-
155) is easily monitored with serial ABGs.
• doesn’t need osmolality testing
• higher reflection coefficient at the blood
brain barrier than mannitol
• can be used as a continuous infusion

DISADVANTAGES:
Need for central venous access
• No standards for which concentration to
use, or how to give it
• Hypokalaemia
• Hyperchloraemic acidosis
• Hypernatremia
• Should not be used if the patient is
chronically hyponatremic
• Phlebitis
• Tissue necrosis if extravasates
• central pontine myelinosis if Na+ corrected
too quickly in hyponatraemia
• Increase in circulating volume with risk of
fluid overload.
• Coagulopathy (APTT and INR)
• Altered platelet aggregation.
• May affect normal brain more that injured
brain which theoretically may worsen
herniation
• Rebound intracranial hypertension