A G Hill, W Teo, A Still, B R Parry, L D Plank, G L Hill
{"title":"Cellular potassium depletion predisposes to hypokalaemia after oral sodium phosphate.","authors":"A G Hill, W Teo, A Still, B R Parry, L D Plank, G L Hill","doi":"10.1046/j.1440-1622.1998.01462.x","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Oral sodium phosphate has become an attractive alternative to polyethylene glycol for colonic cleansing preparatory to elective colorectal surgery. Its use, however, has been associated with hypokalaemia. The authors of the present study tested the hypothesis that patients with cellular depletion of potassium are at significant risk for hypokalaemia with oral sodium phosphate bowel preparation.</p><p><strong>Methods: </strong>In 23 patients, total body potassium was measured by whole-body counting and intracellular water volume was measured by bioimpedance analysis before oral sodium phosphate bowel preparation. Patients were divided into those whose serum potassium fell to 3.5 mmol/L or lower (Group 1) and those whose did not after sodium phosphate treatment (Group 2).</p><p><strong>Results: </strong>The fall in serum potassium concentration over the period of oral sodium phosphate administration was significantly negatively correlated with intracellular potassium concentration measured prior to administration (r = -0.65, P = 0.0009). In Group 1, serum potassium concentration fell from 4.1+/-0.1 (standard error of the mean (SEM)) mmol/L to 3.2+/-0.1 mmol/L (P < 0.0001) while in Group 2 there was no significant change in this concentration (4.0+/-0.1 vs 3.9+/-0.1 mmol/L) as a result of sodium phosphate treatment. Intracellular potassium concentration prior to administration of sodium phosphate was significantly lower in Group 1 (117+/-9 mmol/L vs 143+/-7 mmol/L, P < 0.05).</p><p><strong>Conclusions: </strong>Caution should be exercised when treating patients with oral sodium phosphate who are considered to be cellularly depleted of potassium. These patients are at risk of hypokalaemia after this treatment.</p>","PeriodicalId":22494,"journal":{"name":"The Australian and New Zealand journal of surgery","volume":"68 12","pages":"856-8"},"PeriodicalIF":0.0000,"publicationDate":"1998-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Australian and New Zealand journal of surgery","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1046/j.1440-1622.1998.01462.x","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 2
Abstract
Background: Oral sodium phosphate has become an attractive alternative to polyethylene glycol for colonic cleansing preparatory to elective colorectal surgery. Its use, however, has been associated with hypokalaemia. The authors of the present study tested the hypothesis that patients with cellular depletion of potassium are at significant risk for hypokalaemia with oral sodium phosphate bowel preparation.
Methods: In 23 patients, total body potassium was measured by whole-body counting and intracellular water volume was measured by bioimpedance analysis before oral sodium phosphate bowel preparation. Patients were divided into those whose serum potassium fell to 3.5 mmol/L or lower (Group 1) and those whose did not after sodium phosphate treatment (Group 2).
Results: The fall in serum potassium concentration over the period of oral sodium phosphate administration was significantly negatively correlated with intracellular potassium concentration measured prior to administration (r = -0.65, P = 0.0009). In Group 1, serum potassium concentration fell from 4.1+/-0.1 (standard error of the mean (SEM)) mmol/L to 3.2+/-0.1 mmol/L (P < 0.0001) while in Group 2 there was no significant change in this concentration (4.0+/-0.1 vs 3.9+/-0.1 mmol/L) as a result of sodium phosphate treatment. Intracellular potassium concentration prior to administration of sodium phosphate was significantly lower in Group 1 (117+/-9 mmol/L vs 143+/-7 mmol/L, P < 0.05).
Conclusions: Caution should be exercised when treating patients with oral sodium phosphate who are considered to be cellularly depleted of potassium. These patients are at risk of hypokalaemia after this treatment.