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Indications and Dosage
Intravenous
Source of sodium Adult: For addition to large volume IV fluids for treatment or prevention of hyponatraemia in patients with restricted or no oral intake. Dose and rate of administration are dependent on patient's needs. Maintenance electrolyte requirements of sodium in parenteral nutrition solutions: 1-2 mEq/kg/24 hours. Monitor serum sodium levels for dosage adjustments.
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Reconstitution
Dilute in a larger volume of fluid (e.g. dextrose 5% inj, nutritional admixtures) before administration.
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Contraindications
Hypernatraemia, fluid retention, metabolic or respiratory alkalosis, hypocalcaemia.
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Special Precautions
Patient with acid-base alterations, oedematous or sodium-retaining state, heart failure, cirrhosis, oliguria, anuria. Patient receiving corticosteroid or corticotropin. Avoid extravasation. Renal and severe hepatic impairment. Elderly. Pregnancy.
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Adverse Reactions
Significant: Hypernatraemia; fluid and/or solute overloading resulting in dilution of other serum electrolyte concentrations, overhydration, congested states, or pulmonary oedema.
Gastrointestinal disorders: Abdominal distention, flatulence. Vascular disorders: Localised phlebitis, thrombosis. |
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Monitoring Parameters
Monitor serum electrolytes (e.g. sodium, calcium) and serum pH.
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Overdosage
Symptoms: Hypernatraemia (excessive administration of sodium); hypokalaemia and metabolic alkalosis (excessive administration of acetate). Management: Discontinue treatment immediately and initiate corrective measures to reduce increased sodium levels and restore acid-base balance if needed.
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Drug Interactions
May increase the renal clearance of acidic drugs (e.g. salicylates, barbiturates, tetracyclines). May decrease the renal clearance of basic drugs (e.g. amphetamine, quinidine, pseudoephedrine).
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Action
Description:
Mechanism of Action: Sodium plays an important role in controlling the total body water and its distribution. Sodium is the main cation in the extracellular fluid and comprises >90% of total cations. Acetate is an alternate source of bicarbonate by metabolic conversion in the liver. Pharmacokinetics: Metabolism: Acetate ion is metabolised in the liver into bicarbonate. |
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Chemical Structure
 Source: National Center for Biotechnology Information. PubChem Compound Summary for CID 517045, Sodium Acetate. https://pubchem.ncbi.nlm.nih.gov/compound/Sodium-Acetate. Accessed Jan. 26, 2024. |
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Storage
Store between 20-25°C.
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MIMS Class
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ATC Classification
B05XA08 - sodium acetate ; Belongs to the class of electrolyte solutions used in I.V. solutions.
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References
Anon. Sodium Acetate. Lexicomp Online. Hudson, Ohio. Wolters Kluwer Clinical Drug Information, Inc. https://online.lexi.com. Accessed 21/12/2023. Buckingham R (ed). Bicarbonate. Martindale: The Complete Drug Reference [online]. London. Pharmaceutical Press. https://www.medicinescomplete.com. Accessed 30/06/2023. Sodium Acetate Injection, Solution, Concentrate (Hospira, Inc.). DailyMed. Source: U.S. National Library of Medicine. https://dailymed.nlm.nih.gov/dailymed. Accessed 21/12/2023. Sodium Acetate Injection, Solution, Concentrate (Woodward Pharma Services LLC). DailyMed. Source: U.S. National Library of Medicine. https://dailymed.nlm.nih.gov/dailymed. Accessed 21/12/2023. Sodium Acetate. Gold Standard Drug Database in ClinicalKey [online]. Elsevier Inc. https://www.clinicalkey.com. Accessed 21/12/2023.
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