1574 Chelators Antidotes and

poisoning. Children absorb considerably more ingested every I 2 hours for 5 days to 10 children with asympto­ lead than adults and are at greater risk of developing toxi­ matic lead poisoning.1 As well as reducing blood-lead con­ Sodium Nitrite · city such as encephalopathy. Some recommend intramus­ centrations, sodium calcium edetate also produced a Azotafi(HiJ Sodu; Du$itall sodnj; E250; Natr!i· nitriS; Natrio cular injection as the preferred route (the intravenous marked fall in the mean plasma-zinc concentration but nitllta,;: Natriurn Nitrit Natrium Nitrosum; NatriumniWet; • . route has been associated with fatalities in some young this rebounded rapidly after the end of treatment. Mean Natriumnitriitti; Natr iumn. itiit; Natriul)1o:nitrit; Natrh.Jmntntt; · i children); however, it is painful and others recommend urinary-zinc excretion increased about seventeenfold dur­ . Nitrit de Sodi; Nitrit de Sodru; Nltrito de S6dio; Nitrite de the intravenous route where possible. Last available gui­ ing the first 24 hours of therapy. Sodium calcium edetate Sodio;Nitrito di Sodio; Nitrito Nitrito;Sodium; dance from the American Academy of Pediatrics considered had little effect on the plasma concentrations or urinary nitrite . · azot)lfl; that intravenous administration was safe and more appro­ excretion of copper. The results suggested that careful rie; Sodu. • Sod)'\.tm Htrrpl'l'!; A3orvrcToKY:c%rii priate than the intramuscular route in children; slow infu­ monitoring of zinc was required during treatment with HawMtr. sion over several hours or a continuous infusion were sodium calcium edetate. NaN(),=68.99 recommended.1 Doses are similar to those used in adults, l. Thomas DJ, Chisolm JJ. Lead, zinc and copper decorporation during c�s_,.:: 7632-oo-o. see p. 1573.3. calcium disodium ethylenediamine tetraacctate treatment of" lead­ ATC--,V0 3A808. poisoned children. J Pharmacol Exp Ther 1986; 239: 829-35. 1. Anonymous. Treatment guidelines for lead exposure in children. f\TC Ve t-QVOJAB()$. American Academy of Pediatrics Committee on Drugs. Pediatrics 1995; UNit .'-c MOKG633DIIP. 96; 155-60. {Retired October 2007] Also available at: http://pediatrics. aappublications.org/cgi/reprint/96/1/155 (accessed 31/08/10) Pharmacokinetics Pharmacopoeias. In Chin., Eur. (see p. vii), Int., and US. Sodium calcium edetate is poorly absorbed from the Ph. Eur. 8: (Sodium Nitrite). Hygroscopic. colourless crystals Administration in renal impairment. The dose of sodium gastrointestinal tract. It distributes mainly to the or mass, or yellowish rods. Freely soluble in water; soluble calcium edetate should be reduced in patients with mild extracellular fluid and does not penetrate cells. It is not in alcohol. Store in airtight containers. renal impairment and it should not be used in patients significantly metabolised but is excreted by the kidneys. The USP 36: (Sodium Nitrite). A white to slightly yellow with active renal disease or during periods of anuria. In half-life is about 20 to 60 minutes, with about 50% of a dose adults with lead nephropathy. the following daily intra­ is excreted in the urine in I hour and over 95% in 24 hours. granular powder, or white or practically white, opaque I venous or intramuscular doses have been suggested, fused masses or sticks. It is deliquescent in air. Soluble in 1.5 of water; sparingly soluble in alcohol. Its solutions are according to serum-creatinine concentrations: r t P.r.�P.�. � i?n.� alkaline to litmus. Store in airtight containers at a 20 to 30 micrograms/mL: 500 mg/m2 daily for 5 days Proprietary Preparations (details are given in Volume B) temperature of 25 degrees, excursions permitted between 30 to 40 micrograrns/mL: 500mg/m2 every 48 hours for 3 • doses Single-ingredient Preparations. Gr.: Ledclair; India: Ledcure; Irl.: 15 degrees and 30 degrees. above 40 micrograms/mL: 500 1ng/m2 once weekly Ledclairt; Turk.: Libenta; UK: Ledclair. • These regimens may be repeated at one month intervals. Multi-ingredient Preparations. Arg.: Calcium C. Uses and Administration Pharmacopoeial Preparations Sodium nitrite is used with sodium thiosulfate in the Adverse Effects BP Sodium Caldum Edetate Infusion; 2014: treatment of severe cyanide poisoning (p. 2156.2). Sodium USP 36: Edetate Calcium Disodium Injection. Sodium calcium edetate is nephrotoxic and glycosuria, nitrite produces methaemoglobin which preferentially proteinuria, and microscopic haematuria may occur; renal combines with cyanide ions to form cyanmethaemoglobin, proximal tubular necrosis has resulted in fatal nephrosis. thereby displacing cyanide from cytochrome oxidase . and Glomerular changes occur rarely. Nephrotoxicity appears to Sodium Cellulose Phosphate restoring aerobic metabolism. As cyanide dissociates from be dose dependent. Thrombophlebitis has followed intra­ Cellulose Sodium Phosphat£;.' (USI\N); methaemoglobin, it is converted to relatively non-toxic venous infusion, particularly if given rapidly or if a thiocyanate which is excreted in the urine; sodium :>(idi<:o.de; $o.�¢"aT· HaTf)vtR concentrated solution is used. Pain at the intramuscular Lte}"IJ1!0no3bl thiosulfate is given as a sulfur donor, accelerating the . 9038c41-9; 68444·$8-6 injection site has been reported. Other adverse effects that (AS.-:- conversion of cyanide to thiocyanate. Sodium nitrite may have been reported include gastrointestinal disturbances AT� -:- Y03{\Gq1 ATC \le t . Q\103AG0 1. also enhance cyanide clearance by vasodilatation. such as nausea and diarrhoea, abdominal pain, chills, fever, "- The usual dosage regimen is 300 mg of sodium nitrite VN/1--::- £6S UvJ4Y5Q malaise, headache, myalgia, arthralgia, histamine-like (I0 mL of a 3% solution) given intravenously over 2 to 20 responses such as sneezing, nasal congestion, and lachrym­ Pharmacopoeias. In US. minutes followed by 12.5 g of sodium thiosulfate (50mL of a ation, transient hypotension, cardiac rhythm irregularities, USP 36: (Cellulose Sodium Phosphate). It is prepared by the 25% solution or 25 mL of a 50% solution) given mild increases in hepatic enzyme values, tremor, numbness, IO phosphorylation of alpha cellulose. A free-flowing, cream­ intravenously over minutes. The methaemoglobin tingling, cheilosis, rash, transient bone marrow depression, coloured, odourless, powder. Insoluble in water, in dilute concentration should not be allowed to exceed 30 to 40%. If anaemia, and excessive thirst. acids, and in most organic solvents. The pH of a filtrate of a symptoms of cyanide toxicity recur, it has been suggested Sodium calcium edetate chelates trace metals such as 5% mixture in water is between 6.0 and 9.0. The inorganic that the injections of nitrite and thiosulfate may be repeated zinc within the body and zinc deficiency has been reported. bound phosphate content is not less than 31.0% and not after 30 minutes at half the initial doses. However. the UK Displacement of calcium from sodium calcium edetate may more than 36.0%; the free phosphate content is not more National Poisons Information Service considers the risk of lead to hypercalcaemia. than 3.5%; and the sodium content is not less than 9.5% methaemoglobinaemia to be excessive with a second dose of and not more than 13.0%, all calculated on the dried basis. sodium nitrite and recommends that only the sodium Effects on the kidneys. Of 130 children with lead poison­ thiosulfate be repeated if necessary. In patients with ing who received chelation therapy with sodium calcium The calcium binding capacity, calculated on the dried basis, is not less than 1.8 mmol per g. anaemia, the sodium nitrite dose should be reduced edetate (25 mg/kg intramuscularly every 12 hours) and according to the haemoglobin concentration. dimercaprol (3 mg/kg intramuscularly every 4 hours) for a For doses in children, see below. total of 5 days, 21 developed clinical evidence of nephro­ Profile Sodium nitrite has also been suggested in the treatment toxicity and in 4 severe oliguric acute renal failure began Sodium cellulose phosphate, the sodium salt of hydrogen sulfide poisoning (seep. 1799.2). 1 or 2 days after chelation therapy was discontinued.1 phosphate ester of cellulose, is a cation-exchange resin Sodium nitrite is used as a rust inhibitor, for example in Nephrotoxicity was probably attributable to the use of sod­ that exchanges sodium ions for calcium and other divalent instrument disinfectants. It is also used as a preservative in ium calcium edetate. cations. When given orally, it binds calcium ions within the foods such as cured meats. Potassium nitrite is also used as a 1. Moel Dl, Kumar K. Reversible nephrotic reactions to a combined 2,3- stomach and intestine to form a non-absorbable complex food preservative. dimercapto-l-propanol and calcium disodium ethylenediaminetetraace­ which is excreted in the faeces. Theoretically a 5 -g dose will tic add regimen in asymptomatic children with elevated blood lead Sodium nitrite generates nitric oxide and is being levels. Pediatrics 1982; 70: 259-62. bind about 350 mg calcium. It has been used in the investigated for the treatment of vasa-occlusive crisis in treatment of absorptive hypercalciuria with recurrent sickle-cell disease, myocardial ischaemic-reperfusion injury, formation of calcium-containing renal calculi (p. 2350.3), and cerebral vasospasm. Precautions and in hypercalcaemia associated with osteopetrosis, Sodium calcium edetate should be used with caution, if at sarcoidosis, idiopathic hypercalcaemia of infancy, and all, in patients with renal impairment (see also Adminis­ vitamin D intoxication. Administration in children. Sodium nitrite is used in chil­ tration in Renal Impairment, above). It is also not Diarrhoea and other gastrointestinal disturbances have dren with sodium thiosulfate for the treatment of cyanide recommended in those with hepatitis. Urinalysis, serutn been reported with sodium cellulose phosphate. It should poisoning. The usual regimen for children from 1 month I electrolytes, and renal and hepatic function should be not be given to patients with primary or secondary to 18 years is sodium nitrite 4 to 0 mg/kg to a maximum monitored frequently during treatment. ECG monitoring is hyperparathyroidism, hypomagnesaemia, hypocalcaemia. of 300 mg (0.13 to 0.33mL/kg of a 3% solution. maximum recommended during intravenous therapy. bone disease, or enteric hyperoxaluria, and it should be used 10 mL) by intravenous injection over 5 to 20 minutes, fol­ Sodium calcium edetate can chelate several endogenous cautiously in pregnant women and children, since they lowed by sodium thiosulfate 400 mg/kg to a maximum of 12.5 g (as a 25 or 50% solution) by intravenous injection metals, including zinc, and may increase their excretion; have high calcium requirements. Patients should be I therapy should be intermittent to prevent severe deficiency monitored for electrolyte disturbances. over 0 minutes. US licensed product information suggests developing and monitoring of zinc levels may be required a lower dose of sodium thiosulfate 250 mg/kg (as a 25% (see below). Interactions. Sodium cellulose phosphate binds with cal­ solution), and warns that neonates and infants under 6 Sodium calcium edetate should not be given orally in the cium and other cations. Use with calcium or magnesium months of age may be particularly susceptible to treatment of lead poisoning as it has been suggested that salts, including cation -donating antacids or laxatives, may methaemoglobinaemia with sodium nitrite. As in adults absorption of lead may be increased as a result. reduce its efficacy. Magnesium supplements are often (see Uses. above), doses may need to be reduced in chil­ required in patients receiving sodium cellulose phosphate dren with anaemia. Pregnancy. Although data are scarce, there are reports of hut should be given at least one hour before or after any the use of sodium calcium edetate for poisoning in the sec­ dose of the resin since the absorption of the magnesium ond or third trimester of pregnancy, without adverse may otherwise be impaired. Adverse Effects and Precautions effects on the neonate.u Sodium nitrite may cause nausea and vomiting, abdominal 1. Shannon M. Severe lead poisoning in pregnancy. Ambul Pediatr 2003; 3: P..r�P.�.r�_ti?.n.� pain, dizziness, headache, cyanosis, tachypnoea, and 37-9. dyspnoea. Blurred vision, confusion, anxiety, diaphoresis, 2. Bailey B. Are there teratogenic risks associated with antidotes used in Proprietary Preparations (details are given in Volume B) the acute management of poisoned pregnant women? Birlh Defects Res A fatigue, and generalised numbness or tingling have also Clin Mol Terato/ 2003; 67: 133-40. Single-ingredient Preparations. USA: Calcibindt. been reported. Vasodilatation has resulted in syncope, Pharmacopoeial Prepara6ons hypotension, and tachycardia; arrhythmias, cardiovascular Trace metal depletion. Sodium calcium edetate USP 36: Cellulose Sodium Phosphate for Oral Suspension. collapse, coma, convulsions, and death have occurred in 500 mg/m2 was given by deep intramuscular injection overdose.

All cross-references refer to entries in Volume A Sodium Cellulose Phosphate/Sodium PolysJyrene Sulfonate 1575

Nittites readily oxidise haemoglobin to methaemoglobin, causing methaemoglobinaemia. Methaemoglobin concen­ Adverse Effects and Treatment trations should be monitored and oxygen given during Gastric irritation, anorexia, nausea, vomiting, constipation, sodium nitrite treatment. Caution is needed when sodium and occasionally diarrhoea may develop during treatment nitrite is given with other drugs that may cause with sodium polystyrene sulfonate. Constipation may be methaemoglobinaemia such as procaine and sodium severe; large doses in elderly patients, and rectal use, nitroprusside, and when used in patients with, or at high particularly in children, may result in faecal impaction. risk of. methaemoglobinaemia including those with Gastrointestinal concretions have occurred after oral use. congenital methaemoglobin reductase deficiency, neonates Intesrinal necrosis, which may be fatal, and other serious and infants under 6 months of age, and those with pre­ gastrointestinal effects including bleeding, ulceration, existing anaemia; dose reductions should be considered in ischaemic colitis, and perforation have also occurred. If anaemic patients, see Uses and Administration, p. I574.3. constipation develops, sodium polystyrene sulfonate Care is also required in patients with diminished oxygen or treatment should be stopped until normal bowel function cardiovascular reserves such as those with smoke inhalation returns (see also Precautions, below). Serious potassium deficiency can occur with sodium or substantial blood loss. Patients with G6PD deficiency may Pharmacopoeias. In Bur. (see p. vii), Jpn, and US. be at increased risk of haemolysis with sodium nittite. polystyrene sulfonate and signs of severe hypokalaemia Ph. Eur. 8: (Sodium Polystyrene Sulfonate). An almost Blood pressure should be monitored when giving sodium may include irtitability, confusion, ECG abnormalities, white to light brown powder. It contains 9.4 to ll.O% of nittite as rapid injection can cause hypotension. It should be cardiac arrhythmias, and severe muscle weakness. Like used cautiously with other drugs that reduce blood pressure sodium, calculated with reference to the dried substance. other cation -exchange resins, sodium polystyrene sulfonate Each g exchanges 2.8mmol to 3.4mmol of potassium, or volume, or that cause vasodilatation, such as is not totally selective and its use may result in other antihypertensives, diuretics, and phosphodiesterase type-5 calculated with reference to the dried substance. Practically electrolyte disturbances such as hypocalcaemia and hypo­ inhibitors. Sodium nittite is excreted by the kidneys and insoluble in water, in alcohol. and in dichloromethane. magnesaemia. Significant soclium retention may also occur. care is needed when using in patients with renal Store in airtight containers. impairment. USP 36: (Sodium Polystyrene Sulfonate). A golden brown, Effects on the gostrainlestinol lrad. Colonic necrosis, fine, odourless powder containing not more than l 0% of including some fatalities, has been reported1·3 after use of Carcinogenicity. Sodium nitrite is a precursor for the for­ water. The sodium content is not less than 9.4% and not enemas containing sodium polystyrene sulfonate in sorbi­ mation of N�nitroso compounds such as nitrosamines, more than 11.5%, calculated on the anhydrous basis. Each g tol. Studies in animals1 suggested that the use of sorbitol many of which are carcinogenic in animals. However, data exchanges not less than llOmg and not more than l35mg was a contributory factor, although failure to irtigate the in humans are limited. Occupational exposure to sodium of potassium, calculated on the anhydrous basis. Insoluble colon adequately, as recommended by the manufacturer, nitrite has been associated with a higher incidence of in water. was also suggested4·5 as a possible cause. Both colonic6·7 oesophageal cancer. Sodium nitrite was used as an antic­ and upper gastrointestinal necrosis8 have also been orrosive and coolant fluid in the production of screws, and reported after oral or nasogastric sodium polystyrene sul­ workers were required to blow excess sodium nittite solu­ Uses and Administration fonate with sorbitol, and there have also been reports of lion from screws and so their faces, respiratory tract and Sodium polystyrene sulfonate, the sodium salt of sulfonated colonic necrosis with oral' or rectaJl0 sodium polystyrene alimentary tract were directly exposed; their hands were styrene copolymer with divinylbenzene, is a cation­ sulfonate alone. also soaked in sodium nitrite solution for 8 hours each exchange resin that exchanges sodium ions for potassium I. Lillemoe KD, et al. Intestinal necrosis due to sodium polystyrene day. A cohort of 160 workers were exposed for between ions and other cations in the gastrointestinal tract when (Kayexalate) in sorbitol enemas: clinical and experimental support for 16 and 23 years with 21 developing cancer, including ll the hypothesis. Surgery 1987; 101: 267-72. given orally or rectally. The exchanged resin is then et al. cases of oesophageal cancer, in the 30 years of follow-up; 2. Wootton Ff, Colonic necrosis with Kayexalate-sorbitol enemas excreted in the faeces. Each gram of resin exchanges about after renal transplantation. Ann InternMed 1989; Ill: 947-9. there were no malignancies in a cohort of other unex­ 3 mmol of potassium in vitro, and about l mmol in vivo. 3. Rogers FB, Li SC. Acute colonic necrosis associated with sodium posed workers from the same factory.1 polystyrene sulfonate (Kayexalate) enemas in a critically ill patient: case Sodium polystyrene sulfonate is used to enhance 51: I. Xie T-P, et a!. Long-term exposure to sodium nitrite and risk of report and review of the literature. J Trauma 2001; 395-7. potassium excretion in the treatment of hyperkalaemia, Ann Intern Med esophageal carcinoma: a cohort study for 30 years. DisEsophagus 2011; 4. Burnett RJ. Sodium polystyrene-sorbitol enemas. 1990; Ill: l4: 30-2. including that associated with anuria or severe oliguria, and 31 1-12. in dialysis patients (caution is required due to the sodium 5. Shepard KV. Cleansing enemas after sodium polystyrene sulfonate Ill: content). An effect may not be evident for several hours or enemas. Ann InternMed 1990; 711. Methoemoglobinoemia. Severe methaemoglobinaemia 6. Rashid A. Hamilton SR. Necrosis of the gastrointestinal tract in uremic has been reported after consumption of nitrite-contami­ longer, and in severe hyperkalaemia, where a rapid effect is patients as a result of sodium polystyrene sulfonate (Kayexalate) in nated meat, 1"3 inadvertent ingestion of sodium nitrite,4·8 required, other measures must also be considered (see sorbitol: an underrecognized condition. Am J Surg Patho/ 1997; 21: 60-9. p. 1777.1). 7. McGowan CE, et al. Intestinal necrosis due to sodium polystyrene and intentional overdose.9 lOl: Serum-electrolyte concentrations should be monitored sulfonate (Kayexalate) in sorbitol. South Med J 2009; 493-7. l. Walley T, Flanagan M. Nitrite-induced methaemoglobinaemia. Postgrad 8. Abraham SC, et al. Upper gastrointestinal tract injury in patients Med J 1987; 63: 643-44. throughout treatment and doses given according to receiving kayexalate (sodium polystyrene sulfonate) in sorbitol: clinical 2. Kennedy N, et al. Faulty sausage production causing methaemoglobin­ response. endoscopic, and histopathologic findings. Am J Surg Pathol 2001; l5: aemia. Arch Dis Child 1997; 76: 367-8. The usual oral dose is 15 g up to four times daily as a 637-44. 3. Khan A. et al. Deadly meatballs-a near fatal case of methaemoglobin­ et al. suspension in water or syrup or as a sweetened paste. It 9. Cheng ES, Colonic necrosis and perforation following oral sodium aemia. N Z Med J 2006; 119: U2 1 07. Available at: http://www.nzma.org. polystyrene sulfonate (Resonium A!Kayexelate) in a bum patient. Burns nz/joumalf ll9-l239/2107/content.pdf (accessed 26/01/11) should not be given in fruit juices that have a high 2002; l8: 189-90, 4. Finan A. et al. Methaemoglobinaemia associated with sodium nitrite in potassium content. 10. Rugolotto S, etal. Necrotizing enterocolitis in a 850 gram infant receiving three siblings. BMJ 1998; 317: ll38-9. When oral use is difficult, sodium polystyrene sulfonate sorbitol-free sodium polystyrene sulfonate (Kayexalate): clinical and 5. Anonymous. Methemoglobinemia following unintentional ingestion of histopathologic findings. J Pen'nato/ 2007; l7: 247-9. 51: may be given rectally as an enema. The usual daily dose is sodium nitrite-New York, 2002. MMWR 2002; 639-42. 6. Chui JSW, et al. Nitrite-induced methaemoglobinaemia-aetiology, 30 g given as a suspension in 150 mL of water or glucose diagnosis and treatment. Anaesthesia 2005; 60: 496-500. 10%. The enema should be retained, if possible, for at least 9 Effects on the lungs. Particles of sodium polystyrene sulfo­ 7. Tung S-P, et al. Methaemoglobinaemia secondary to the ingestion of hours; higher doses, shorter retention times, and alternative nate were found at autopsy in the lungs of 3 patients who sodium nitrite in mistake for common salt. Resuscitation 2006; 70: 168-9. had taken the resin orally and were associated with acute 8. Marie P, et a!. Methaemoglobinaemia following ingestion of a commonly vehicles have also been. used. After retention of the enema available food additive. Med J Aust 2008; 188: 156-8. the colon should be irtigated to remove the resin. Initial bronchitis and bronchopneumonia in 2 and with early 9. Harvey M, et al. Fatal methaemoglobinaemia induced by self-poisoning therapy may involve both oral and rectal routes. bronchitis in the third.1 It was suggested that, where possi­ with sodium nitrite. Bmerg Med Australas 2010; ll: 463-5. For doses in children, see below. ble, it may be preferable to give sodium polystyrene sulfo­ Other polystyrene sulfonate resins include calcium nate rectally, but if it has to be given orally the patient Treatmentof AdverseEffects polystyrene sulfonate (p. 1541.2), which is used similarly to should be positioned carefully to avoid aspiration. the sodium resin and potassium polystyrene sulfonate, 1. Haupt HM, Hutchins GM. Sodium polystyrene sulfonate pneumonitis. When toxicity results from the ingestion of nitrites, 142: which has been used in the treatment of hypercalciuria. Arch InternMed 1982; 379-8 1. treatment is supportive and symptomatic; oxygen and Aluminium polystyrene sulfonate, ammonium polystyrene methylthioninium chloride may be required for methaemo­ sulfonate, and magnesium polystyrene sulfonate have all globinaemia although methylthioninium chloride should Precautions occasionally been used. not be given if cyanide poisoning is suspected since cyanide Sodium polystyrene sulfonate should not be given orally to may be displaced. Exchange transfusion may be considered neonates, and is contra-indicated by any route in those with for severe or refractory methaemoglobinaemia. Administration in children. Sodium polystyrene sulfonate reduced gut motility or obstructive bowel disease. Care is is used in neonates and children to enhance potassium also needed with rectal use in neonates and children in Pharmacokinetics excretion in the treatment of hyperkalaemia, including order to avoid impaction of the resin. Treatment should be that associated with anuria or severe oliguria, and in stopped if clinically significant constipation develops. Sodium nittite is rapidly absorbed after oral dosing. In the dialysis patients. It may be given orally as a suspension or Although sorbitol has been recommended for the prophy­ blood nitrite reacts with haemoglobin, producing methae­ paste (see above), or rectally. Each l g of sodium poly­ laxis and treatment of constipation, there have been reports moglobin; the peak effect is seen about 30 to 70 minutes styrene sulfonate to be given rectally is mixed with 5 to of colonic necrosis, including fatalities, in patients given this after an intravenous dose. About 40% of a dose of sodium I 0 mL of a methylcellulose solution; 5 mL water or glucose combination (see Effects on the Gastrointestinal Tract, nittite is excreted unchanged in the urine, with the 10% may also be used but retention is more difficult. above) and most licensed product information advises remaining 60% metabolised to ammonia and similar small With rectal use the enema should be retained as long as against the use of sorbitol with polystyrene sulfonates. molecules. Elimination half-life ranges from 21 minutes possible and the colon then irtigated to remove the resin. Magnesium-containing laxatives are also contra-indicated (intravenous dosing) to 35 minutes (oral ingestion). Care is needed with rectal use in children as excessive (see Interactions, p. 1576. 1). dosage or inadequate dilution can result in impaction of Patients receiving sodium polystyrene sulfonate should �!�f:"'!<:l�i?,��...... the resin; however, the oral route is not recommended in be monitored for electrolyte disturbances, especially Proprietary Preparations (details are given in Volume B) neonates. hypokalaemia. Since serum concentrations may not always UK licensed product information recommends a dose of reflect intracellular potassium deficiency, symptoms of Multi-ingredient Preparations. Gr.: Cyanide Antidote Package; l g/kg daily in divided doses, reduced to a maintenance dose hypokalaemia should also be watched for and the decision Ital.: Citrosil Alcolico Azzuro; S.Afr.: Tripac-Cyano; USA: Cya­ of 500 mg/kg daily in divided doses. Alternatively, the BNFC to stop treatment assessed individually. nide Antidote Package; Nithiodote. suggests doses of 125 to 250mg/kg three or four times daily; Use of sodium polystyrene sulfonate can result in sodium Pharmacopoeial Preparations the maximum single dose via the oral route is 15 g. In the overloading and it should be used cautiously in patients USP 36: Sodium Nitrite Injection. USA licensed product information suggests I g of sodium with renal failure or conditions requiring a restricted polystyrene sulfonate for each mmol of potassium. sodium intake, such as heart failure and severe hyper-

The symbol t denotes a preparation no longer actively marketed