Sodium Lactate

(rINNM)

💊 Chemical information

E325; Lactato de sodio; Natrii lactatis; Natriumlaktaatti; Natriumlaktat; Sodium, lactate de. Sodium 2-hydroxypropionate.
Chemical formula: C3H5NaO3 = 112.1.
CAS — 72-17-3.

Pharmacopoeias.

Chin., Eur., and US include preparations of sodium lactate.

Ph. Eur. 6.2

(Sodium Lactate Solution). It contains a minimum of 50% w/w of sodium lactate and is a mixture of the two enantiomers in about equal proportions. Sodium (S)-Lactate Solution contains a minimum of 50% w/w of sodium lactate, not less than 95% of which is the (S)-enantiomer. The solutions are clear, colourless, slightly syrupy liquids. Miscible with water and with alcohol. pH 6.5 to 9.0.

USP 31

(Sodium Lactate Solution). It is an aqueous solution containing at least 50% sodium lactate. A clear, colourless or practically colourless, slightly viscous liquid, odourless or having a slight, not unpleasant, odour. Miscible with water. pH between 5.0 and 9.0. Store in airtight containers.

Equivalence.

Each g of sodium lactate (anhydrous) represents about 8.9 mmol of sodium and of lactate. Sodium lactate (anhydrous) 4.88 g is equivalent to about 1 g of sodium.

💊 Adverse Effects and Treatment

Excessive use of bicarbonate or bicarbonate-forming compounds may lead to hypokalaemia and metabolic alkalosis, especially in patients with impaired renal function. Symptoms include mood changes, tiredness, slow breathing, muscle weakness, and irregular heartbeat. Muscle hypertonicity, twitching, and tetany may develop, especially in hypocalcaemic patients. Treatment of metabolic alkalosis associated with bicarbonate overdose consists mainly of appropriate correction of fluid and electrolyte balance. Replacement of calcium, chloride, and potassium ions may be of particular importance. Excessive doses of sodium salts may also lead to sodium overloading and hyperosmolality. Sodium bicarbonate given orally can cause stomach cramps, belching, and flatulence. Extravasation of irritant hypertonic sodium bicarbonate solutions resulting in local tissue necrosis has been reported after intravenous dosage. Excessive doses of potassium salts may lead to hyperkalaemia. Ingestion of potassium salts can cause gastrointestinal adverse effects, and tablet formulations may cause contact irritation due to high local concentrations of potassium. Excessive oral doses of citrate salts may have a laxative effect.

Effects on the gastrointestinal tract.

In addition to minor gastrointestinal effects (see above), spontaneous rupture of the stomach, although an exceedingly rare event, has been reported on several occasions after ingestion of sodium bicarbonate. The bicarbonate was believed to have resulted in the rapid production of enough carbon dioxide to rupture a stomach already distended with food, liquid, or air.1,2
1. Mastrangelo MR, Moore EW. Spontaneous rupture of the stomach in a healthy adult man after sodium bicarbonate ingestion. Ann Intern Med 1984; 101: 649
2. Lazebnik N, et al. Spontaneous rupture of the normal stomach after sodium bicarbonate ingestion. J Clin Gastroenterol 1986; 8: 454–6.

Effects on mental state.

Sodium lactate infusions have been reported to induce panic attacks, especially in patients with anxiety states, and have been used as a pharmacological model in the evaluation of mechanisms involved in panic disorder.1 However, the mechanism that underlies panic attacks induced by lactate remains unknown,1 and it has been suggested2 that rapid administration of the large sodium load may be involved. There has also been a report3 of a patient receiving oral lactate (as calcium lactate) who was suffering from panic disorder associated with agoraphobia; when lactate was discontinued, the patient reported a reduction in panic intensity without a decrease in the frequency of attacks.
1. Bourin M, et al. Provocative agents in panic disorder. Therapie 1995; 50: 301–6
2. Peskind ER, et al. Sodium lactate and hypertonic sodium chloride induce equivalent panic incidence, panic symptoms, and hypernatremia in panic disorder. Biol Psychiatry 1998; 44: 1007–16
3. Robinson D, et al. Possible oral lactate exacerbation of panic disorder. Ann Pharmacother 1995; 29: 539–40.

Epileptogenic effect.

Alkalosis may precipitate seizures; however, absence seizures have also been reported to be associated with sodium bicarbonate administration in a child in whom the serum pH was normal.1
1. Reif S, et al. Absence seizures associated with bicarbonate therapy and normal serum pH. JAMA 1989; 262: 1328–9.

💊 Precautions

Bicarbonate or bicarbonate-forming compounds should not generally be given to patients with metabolic or respiratory alkalosis, hypocalcaemia, or hypochlorhydria. During treatment of acidosis, frequent monitoring of serum-electrolyte concentrations and acid–base status is essential. Sodium-containing salts should be given extremely cautiously to patients with heart failure, oedema, renal impairment, hypertension, eclampsia, or aldosteronism. Potassium-containing salts should be given with considerable care to patients with renal or adrenocortical insufficiency, cardiac disease, or other conditions that may predispose to hyperkalaemia.

Abuse.

High doses of bicarbonate have been taken by athletes to enhance performance in endurance sports by buffering hydrogen ions produced in conjunction with lactic acid.1 Bicarbonates have also been used to alkalinise the urine and prolong the halflife of basic drugs, notably sympathomimetics and stimulants, thereby avoiding detection; however, such a practice may enhance toxicity.
1. Kennedy M. Drugs and athletes—an update. Adverse Drug React Bull 1994; (Dec): 639–42.

💊 Interactions

The effect of oral bicarbonate or bicarbonate-forming compounds in raising intra-gastric pH may reduce or increase the rate and/or extent of absorption of a number of drugs. Alkalinisation of the urine leads to increased renal clearance of acidic drugs such as salicylates, tetracyclines, and barbiturates. Conversely, it prolongs the half-life of basic drugs and may result in toxicity (see also under Abuse, above). Sodium bicarbonate enhances lithium excretion. The use of potassium-containing salts with drugs that increase serum-potassium concentrations such as ACE inhibitors and potassium-sparing diuretics should generally be avoided. Citrate salts taken orally can enhance the absorption of aluminium from the gastrointestinal tract. Patients with impaired renal function are particularly susceptible to aluminium accumulation and citrate-containing oral preparations, including many effervescent or dispersible tablets, are best avoided by patients with renal failure taking aluminium-containing compounds.

💊 Pharmacokinetics

Oral bicarbonate, such as sodium bicarbonate, neutralises gastric acid with the production of carbon dioxide. Bicarbonate not involved in that reaction is absorbed and in the absence of a deficit of bicarbonate in the plasma, bicarbonate ions are excreted in the urine, which is rendered alkaline, and there is an accompanying diuresis. Acetates such as potassium acetate and sodium acetate, citrates such as potassium citrate, sodium acid citrate, and sodium citrate, and lactates such as sodium lactate are metabolised, after absorption, to bicarbonate.

💊 Uses and Administration

Bicarbonate-providing salts are alkalinising agents used for a variety of purposes including the correction of metabolic acidosis, alkalinisation of the urine, and as antacids. When an alkalinising agent is indicated for treating acute or chronic metabolic acidosis, sodium bicarbonate is usually used. In conditions when acute metabolic acidosis is associated with tissue hypoxia, such as cardiac arrest and lactic acidosis, the role of such alkalinising agents is controversial. Sodium lactate has been given as an alternative to sodium bicarbonate in acute metabolic acidosis, but is no longer recommended because of the risk of precipitating lactic acidosis. In chronic hyperchloraemic acidosis associated with potassium deficiency, potassium bicarbonate may be preferred to sodium bicarbonate. The citrate salts of potassium or sodium have also been used as alternatives to sodium bicarbonate in treating chronic metabolic acidosis resulting from renal disorders. Sodium bicarbonate, lactate and acetate, and potassium acetate are used as bicarbonate sources in dialysis fluids. The dose of bicarbonate required for the treatment of acidotic states must be calculated on an individual basis, and is dependent on the acid–base balance and electrolyte status of the patient. In the treatment of chronic acidosis bicarbonate has been given orally and doses providing 57 mmol (4.8 g sodium bicarbonate) or more daily may be required. In severe acidosis, sodium bicarbonate has been given intravenously by continuous infusion usually as a 1.26% (150 mmol/litre) solution or by slow intravenous injection of a stronger (hypertonic) solution of up to 8.4% (1000 mmol/litre) sodium bicarbonate. For the correction of acidosis during advanced cardiac life support procedures, doses of 50 mmol of sodium bicarbonate (50 mL of an 8.4% solution) may be given intravenously to adults. Frequent monitoring of serum-electrolyte concentrations and acid–base status is essential during treatment of acidosis. Sodium bicarbonate may be used in the management of hyperkalaemia to promote the intracellular uptake of potassium and correct associated acidosis, although there is some debate as to its value. Some sources suggest that 50 to 100 mL of an 8.4% solution may be given in severe hyperkalaemia accompanied by acidosis, although more dilute solutions have been used, and care is required, particularly if there is accompanying renal impairment. Sodium bicarbonate, sodium citrate, and potassium citrate cause alkalinisation of the urine. They may therefore be given to relieve discomfort in mild urinary-tract infections and to prevent the development of uric-acid renal calculi in the initial stages of uricosuric therapy for hyperuricaemia in chronic gout. In both cases, they are given with a liberal fluid intake, usually by mouth, in divided doses of up to about 10 g daily. Sodium bicarbonate may also be used to alkalinise the urine in acute poisoning with weakly acidic drugs such as salicylates and phenoxyacetate pesticides; use with a diuretic for ‘forced alkaline diuresis’ is no longer recommended. When given orally, sodium bicarbonate and potassium bicarbonate neutralise acid secretions in the gastrointestinal tract and sodium bicarbonate in particular is therefore frequently included in antacid preparations. To relieve dyspepsia doses of about 1 to 5 g of sodium bicarbonate in water have been taken when required. Sodium citrate has been widely used as a ‘clear’ (non-particulate) antacid, usually with an H 2 antagonist, for the prophylaxis of acid aspiration associated with anaesthesia. Sodium bicarbonate is also used in various preparations for double-contrast radiography where production of gas (carbon dioxide) in the gastrointestinal tract is necessary. Similarly, solutions containing sodium bicarbonate or citrate have been used to treat acute oesophageal impaction. Sodium bicarbonate and sodium or potassium citrate are used as buffering or alkalinising agents in pharmaceutical formulation. Sodium or potassium bicarbonate and anhydrous sodium citrate are used in effervescent tablet formulations. Individual salts also have other specific uses. A 5% solution of sodium bicarbonate can be administered as ear drops to soften and remove ear wax. Sodium bicarbonate injection has been used to treat extravasation of anthracycline antineoplastics although as mentioned in Adverse Effects, above, hypertonic solutions may themselves cause necrosis. Sodium citrate has anti-clotting properties and is used, as sodium acid citrate, with other agents in solutions for the anticoagulation and preservation of blood for transfusion purposes. Similarly, sodium citrate 3% irrigation may be useful for the dissolution of blood clots in the bladder as an alternative to sodium chloride 0.9%. Enemas containing sodium citrate are given rectally as osmotic laxatives. Sodium citrate is also a common ingredient in cough mixtures. Eye drops containing sodium citrate 10% have been used in the treatment of chemical eye burns (below); they may be used with potassium ascorbate eye drops.

Eye disorders.

Sodium bicarbonate is used in the management of blepharitis, an inflammation of the margin of the eyelids with various causes. It may be allergic in nature or associated with seborrhoea of the scalp. Infection of the eyelids can produce ulcerative blepharitis, a condition characterised by the formation of yellow crusts which may glue the eyelashes together. Parasites occasionally cause blepharitis. The condition is first treated by cleaning the eyes and eyelids with sodium bicarbonate solution or a suitable bland eye lotion; simple eye ointment or diluted baby shampoo can also be used to soften crusts to aid removal. If an infection is present, antibacterials may be required. Long-term management consists of daily cleansing of the lid margins with a bland eye lotion. EYE BURNS. Both heat and chemicals can burn the eye, causing damage to the conjunctiva, cornea, and underlying structures. Burn severity may be influenced by the amount of burning substance that enters the eye and the duration of contact, its temperature and impact force, whether it is a liquid or solid, its pH, and osmolarity.1,2 Hydrofluoric acid, sulfurous acid, and alkalis readily penetrate the corneal stroma.2 Immediate irrigation is essential, and a duration of at least 15 to 30 minutes is recommended; it may need to be repeated periodically. Water or sodium chloride 0.9% solution may be used initially, but because they are hypotonic to the eye there can be an increased uptake of the fluid and diffusion of the burning substance into the deeper layers of the cornea, resulting in oedema. To reduce this risk solutions with higher osmolarities have been suggested, if available, and include balanced salt solution, buffered solutions such as lactated Ringer’s solution, and commercial decontamination preparations with amphoteric and chelating properties.1,2 For acid and alkali burns ascorbate and citrate eye drops have been tried, and ascorbate given orally, based on suggestions that ascorbate may scavenge free radicals and citrate may reduce the release of free radicals and proteolytic enzymes in burn tissue.1However, a retrospective analysis of 121 patients with alkali burns to the eye suggested those with less severe burns (grades 1 and 2) did not benefit from an intensive topical therapy regimen including 10% ascorbate drops and 10% citrate drops;3 a trend to more rapid healing and better visual outcome were seen in patients with grade 3 burns but in those with the most severe damage (grade 4) the regimen made no difference. In the management of hydrofluoric acid burns of the eye, calcium gluconate has also been used after initial irrigation. Other general treatments that may be required include topical application of anaesthesia, corticosteroids, and antibacterials, treatment for glaucoma, and surgery.1,2
1. Schrage NF, et al. Eye burns: an emergency and continuing problem. Burns 2000; 26: 689–99
2. Kuckelkorn R, et al. Emergency treatment of chemical and thermal eye burns. Acta Ophthalmol Scand 2002; 80: 4–10
3. Brodovsky SC, et al. Management of alkali burns: an 11-year retrospective review. Ophthalmology 2000; 107: 1829–35.

Osteoporosis.

Potassium bicarbonate in an oral dose of 1 to 2 mmol/kg daily improved mineral balance and bone metabolism in a short-term study.1 However, the authors cautioned against the use of bicarbonate to treat or prevent osteoporosis without further study.2
1. Sebastian A, et al. Improved mineral balance and skeletal metabolism in postmenopausal women treated with potassium bicarbonate. N Engl J Med 1994, 330: 1776–81
2. Sebastian A, Morris RC. Improved mineral balance and skeletal metabolism in postmenopausal women treated with potassium bicarbonate. N Engl J Med 1994; 331: 279.

Renal calculi.

Citrate forms soluble complexes with calcium, thereby reducing urinary saturation of stone-forming calcium salts. Potassium citrate has a hypocalciuric effect when given orally, probably due to enhanced renal calcium absorption. Urinary calcium excretion is unaffected by sodium citrate, since the alkali-mediated hypocalciuric effect is offset by a sodium-linked calciuresis.1 Potassium citrate may be beneficial in reducing the rate of stone formation in patients with hypocitraturia2,3 or hypercalciuria.4 As mentioned in Uses above, sodium bicarbonate or sodium or potassium citrate may also be used for their alkalinising action, as an adjunct to a liberal fluid intake, to prevent development of uric-acid renal calculi during uricosuric therapy. Urinary alkalinisation with sodium bicarbonate, sodium citrate, or potassium citrate may be useful in the management of cystine stone formation in patients with cystinuria.
1. Anonymous. Citrate for calcium nephrolithiasis. Lancet 1986; i: 955
2. Pak CYC, Fuller C. Idiopathic hypocitraturic calcium-oxalate nephrolithiasis successfully treated with potassium citrate. Ann Intern Med 1986; 104: 33–7
3. Tekin A, et al. Oral potassium citrate treatment for idiopathic hypocitruria in children with calcium urolithiasis. J Urol (Baltimore) 2002; 168: 2572–4
4. Pak CYC, et al. Prevention of stone formation and bone loss in absorptive hypercalciuria by combined dietary and pharmacological interventions. J Urol (Baltimore) 2003; 169: 465–9.

💊 Preparations

BP 2008: Alginate Raft-forming Oral Suspension; Alkaline Gentian Mixture; Aromatic Magnesium Carbonate Mixture; Compound Magnesium Trisilicate Oral Powder; Compound Sodium Bicarbonate Tablets; Compound Sodium Chloride Mouthwash; Kaolin and Morphine Mixture; Kaolin Mixture; Magnesium Trisilicate Mixture; Potassium Citrate Mixture; Sodium Bicarbonate Ear Drops; Sodium Bicarbonate Eye Lotion; Sodium Bicarbonate Intravenous Infusion; Sodium Bicarbonate Oral Solution; Sodium Citrate Eye Drops; Sodium Citrate Irrigation Solution; Sodium Lactate Intravenous Infusion; BPC 1968: Effervescent Potassium Tablets; Ph. Eur.: Anticoagulant Acid-Citrate-Glucose Solutions (ACD); Anticoagulant Citrate-Phosphate-Glucose Solution (CPD); USP 31: Anticoagulant Citrate Dextrose Solution; Anticoagulant Citrate Phosphate Dextrose Adenine Solution; Anticoagulant Citrate Phosphate Dextrose Solution; Anticoagulant Sodium Citrate Solution; Half-strength Lactated Ringer’s and Dextrose Injection; Lactated Ringer’s and Dextrose Injection; Lactated Ringer’s Injection; Magnesium Carbonate and Sodium Bicarbonate for Oral Suspension; Magnesium Carbonate, Citric Acid, and Potassium Citrate for Oral Solution; Potassium and Sodium Bicarbonates and Citric Acid Effervescent Tablets for Oral Solution; Potassium Bicarbonate and Potassium Chloride Effervescent Tablets for Oral Solution; Potassium Bicarbonate and Potassium Chloride for Effervescent Oral Solution; Potassium Bicarbonate Effervescent Tablets for Oral Solution; Potassium Chloride in Lactated Ringer’s and Dextrose Injection; Potassium Chloride, Potassium Bicarbonate, and Potassium Citrate Effervescent Tablets for Oral Solution; Potassium Citrate And Citric Acid Oral Solution; Potassium Citrate Extended-release Tablets; Potassium Gluconate and Potassium Citrate Oral Solution; Potassium Gluconate, Potassium Citrate, and Ammonium Chloride Oral Solution; Sodium Acetate Injection; Sodium Acetate Solution; Sodium Bicarbonate Injection; Sodium Bicarbonate Oral Powder; Sodium Bicarbonate Tablets; Sodium Citrate and Citric Acid Oral Solution; Sodium Lactate Injection; Sodium Lactate Solution; Tricitrates Oral Solution; Trikates Oral Solution.

Proprietary Preparations

Arg.: LTK250; Urokit; Austral.: Chlorvescent; Sodibic; Urocit-K; Austria: Oxalyt; Uralyt-U; Belg.: Uralyt-U; Braz.: Acalka†; Citrosodine†; Litocit; Canad.: Bromo Seltzer; Eno; K-Citra; K-Lyte; Polycitra-K; Chile: Acalka; Eucerin; Sal De Yasta†; Cz.: Alkaligen†; Uralyt-U; Fr.: Elgydium Bicarbonate†; Potensium gelule; Ger.: Alkala T; Apocit; bicaNorm; Blanel; Kalitrans; Kalium; Kohlensaurebad Bastian; Nephrotrans; Uralyt-U; Gr.: Citrolithin; Hong Kong: Urocit-K; Hung.: Alkaligen; India: Alkasol; Citralka; Oricitral; Irl.: Cystopurin; Israel: Babic; Uralyt-U; Ital.: Citrosodina; Uralyt-U; Jpn: Meylon; Malaysia: Urocit-K; Mex.: Betsol Z; Bicarnat; Debonal; Neth.: Citra-Lock; Hospasol; Norw.: Kajos; NZ: Citravescent; Philipp.: Acalka; Pol.: Citrolyt; Litocid; Port.: Acalka; Hospasol; Uralyt-U; S.Afr.: Crystacit; SB Gripe Water; Uralyt-U; Singapore: Gripe Water†; Urocit-K†; Spain: Acalka; Hospasol; Plurisalina; Swed.: Kajos; Switz.: Nephrotrans; Uralyt-U†; Thai.: Acalka; Uralyt-U; Turk.: Anti-Asidoz; Urocid-K; UK: Boots Gripe Mixture 1 Month Plus; Canesten Oasis; Cymalon Cranberry; Cystitis Relief; Cystocalm; Cystopurin; USA: Citra pH; K + Care†; K-Lyte; Neut; Urocit-K; Venez.: Policitra.
Published October 22, 2018.