Oral Sodium Phosphate Bowel Preparation Research Articles

Acute renal failure following oral sodium phosphate bowel preparation: a nationwide case-crossover study.

Oral sodium phosphate (OSP) is a cleansing agent for colonoscopy. Recent reports have cited an increased risk of acute renal failure (ARF) in OSP bowel purgative users, but this risk remains under debate. This study was performed to evaluate the association between OSP and ARF in patients who underwent colonoscopy. A population-based case-crossover study was conducted using the Korean Health Insurance Review and Assessment Service (HIRA) claims data from 1 January 2005 to 31 December 2009. The study population consisted of patients aged ≥ 50 years who underwent colonoscopies after an OSP prescription prior to their first hospitalization for ARF. For each patient, one hazard and four control periods were matched at specified time windows. Conditional logistic regression analysis was used to estimate the odds ratio (OR) and 95 % confidence interval (CI), adjusting for concomitant medications that could induce ARF. A total of 1105 patients were included (54 % male). The adjusted ORs for ARF related to the use of OSP when applying the 1-, 2-, 4-, 8-, or 12-week time windows were 3.7 (95 %CI 2.37 - 5.67), 3.5 (95 %CI 2.45 - 4.89), 3.0 (95 %CI 2.30 - 3.95), 2.4 (95 %CI 1.93 - 2.96), and 2.0 (95 %CI 1.69 - 2.46), respectively. When adopting an 8-week time window, the adjusted OR was 2.5 (95 %CI 1.98 - 3.16) for the subgroup without chronic renal failure. The use of OSP was significantly associated with ARF both in patients with and without co-morbidities.

Electrolyte Imbalances and Nephrocalcinosis in Acute Phosphate Poisoning on Chronic Type 1 Renal Tubular Acidosis due to Sjögren's Syndrome

Although renal calcium crystal deposits (nephrocalcinosis) may occur in acute phosphate poisoning as well as type 1 renal tubular acidosis (RTA), hyperphosphatemic hypocalcemia is common in the former while normocalcemic hypokalemia is typical in the latter. Here, as a unique coexistence of these two seperated clinical entities, we report a 30-yr-old woman presenting with carpal spasm related to hypocalcemia (ionized calcium of 1.90 mM/L) due to acute phosphate poisoning after oral sodium phosphate bowel preparation, which resolved rapidly after calcium gluconate intravenously. Subsequently, type 1 RTA due to Sjögren's syndrome was unveiled by sustained hypokalemia (3.3 to 3.4 mEq/L), persistent alkaline urine pH (> 6.0) despite metabolic acidosis, and medullary nephrocalcinosis. Through this case report, the differential points of nephrocalcinosis and electrolyte imbalances between them are discussed, and focused more on diagnostic tests and managements of type 1 RTA.

A case of Conn's syndrome revealed after oral sodium phosphate (fleet) preparation for colonoscopy

Oral sodium phosphate solutions (Fleet Mcneil Consumer Healthcare, Guelph, Ontario, Canada) are commonly used as bowel cleansing agents in preparation for colonoscopic exams; however, serious electrolyte disorders associated with oral sodium phosphate use have been described in case reports including hyperphosphatemia, hypocalcemia, hypomagnesemia, hypernatremia, and hypokalemia. We describe a 57-year-old patient with a past history of resistant hypertension who experienced severe symptomatic hypokalemia following colonic cleansing with an oral sodium phosphate solution. Further investigations revealed a serum aldosterone of 691 pmol/L and a serum renin level of 0.02 ng/L/s with a corresponding aldosterone-to-renin ration of 34550:1. The patient was subsequently diagnosed with primary aldosteronism secondary to an adenoma of the adrenal gland. Bilateral adrenal venous sampling revealed excessive levels of aldosterone in the left adrenal vein prior to definitive surgery. This case indicates that an oral sodium phosphate bowel preparation, though safe for most patients, can be complicated by a previously not diagnosed endocrine disease like the primary aldosteronism (Conn's syndrome) reported here. This is the first report of a Conn's syndrome diagnosed after bowel cleansing with a sodium phosphate solution.

Oral sodium phosphate may worsen kidney dysfunction

A retrospective, comparative study that focuses on patients with already impaired kidney function adds to the body of evidence that links administration of oral sodium phosphate bowel-preparation solutions for colonoscopy with a decrease in renal function. When possible, a polyethylene glycol solution should be used instead.

Adverse Renal and Metabolic Effects Associated with Oral Sodium Phosphate Bowel Preparation

Colorectal cancer can be prevented by the removal of adenomatous polyps during screening colonoscopy, but adequate bowel preparation is required. Oral sodium phosphate (OSP), an effective bowel purgative, is available over the counter and requires a substantially lower volume than polyethylene glycol-based preparative agents. Accumulating reports implicate OSP in electrolyte disturbances as well as acute kidney injury (AKI) in a syndrome termed phosphate nephropathy (a form of nephrocalcinosis). Despite published case reports and case series, the actual incidence, risk factors, and natural history of phosphate nephropathy remain largely undefined. Several recent observational studies have provided new information on these important issues while supporting a link between OSP and acute phosphate nephropathy as well as the development of chronic kidney disease in elderly patients, many of whom had a normal serum creatinine at the time of OSP ingestion. This review summarizes current knowledge about the renal complications of OSP, risk factors for its development, and the pathophysiology of acute and chronic kidney damage in nephrocalcinosis.

Acute Renal Failure Following Oral Sodium Phosphate Bowel Preparation in Diabetes

Recently there is renewed interest in the association between type 2 diabetes and colorectal carcinoma (1). Some authorities have advocated more intensive colonoscopy screening in patients with diabetes (2). We recently managed two diabetic patients who developed acute renal failure following elective colonoscopy. The clinical presentation and biochemical parameters of these two patients are summarized in Table 1. Both of the patients described had normal renal function at baseline, yet presented with acute renal failure within a few days following bowel preparation and colonoscopy, thus strongly implicating the bowel preparation in the development of the acute renal failure. Both patients …

Predictors of inadequate bowel preparation for colonoscopy

OBJECTIVE: Inadequate preparation of the bowel for colonoscopy can result in both missed pathological lesions and cancelled procedures. We looked prospectively at the quality of colonic preparation and evaluated potential associations between specific patient characteristics and inadequate colonic preparation. METHODS: Data were gathered on consecutive patients presenting for colonoscopy who received either a polyethylene glycol lavage or oral sodium phosphate bowel preparation. Patient demographic and medical history information was gathered before scheduled colonoscopy. The endoscopist evaluated the preparation quality during the procedure. Complete data were gathered on 649 of 714 eligible patients (90.8%). Possible predictors of inadequate colonic preparation were analyzed using univariate statistics and multivariate logistic regression models. RESULTS: An inadequate colonic preparation was reported in 21.7% of observed colonoscopies. Only 18% of patients with an inadequate colonic preparation reported a failure to adequately follow preparation instructions. A later colonoscopy starting time, a reported failure to follow preparation instructions, inpatient status, a procedural indication of constipation, taking tricyclic antidepressants, male gender, and a history of cirrhosis, stroke or dementia were all independent predictors of an inadequate colon preparation (all p < 0.05). A procedural indication of previous polypectomy was a negative predictor of inadequate colonic preparation ( p < 0.05). CONCLUSION: Several patient characteristics were significantly associated with colonic preparation quality independent of preparation type, compliance with preparation instructions, and procedure starting time. This information may help to identify patients at an increased risk for inadequate colonic preparation for whom alternative preparation protocols would be appropriate.

Cellular potassium depletion predisposes to hypokalaemia after oral sodium phosphate.

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. 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). 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). 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.

CELLULAR POTASSIUM DEPLETION PREDISPOSES TO HYPOKALAEMIA AFTER ORAL SODIUM PHOSPHATE

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 &lt; 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.

Colorectal inflammation and increased cell proliferation associated with oral sodium phosphate bowel preparation solution

Evidence is emerging that sodium phosphate (NaP), a commonly used oral cathartic agent, causes aphthoid ulcers or focal active colitis (FAC) in the colon and rectum. The aims of this study were (1) to assess the incidence of such ulcers diagnosed endoscopically (“aphthoid ulcers”), (2) to assess the incidence of histologically detected FAC and neutrophilic infiltration overlying lymphoid follicles (“aphthoid lesions”), and (3) to determine whether this effect of NaP is associated with epithelial cell proliferation. Aphthoid ulcers, unexplained by other diagnoses, were found in 18 of 687 consecutive patients (2.6%) who underwent colonoscopic examination after oral NaP preparation during a 12-month period; biopsy specimens showed FAC or aphthoid lesions. FAC was present in 11 of 316 patients (3.5%) who had biopsies but were endoscopically normal. Eight patients with aphthoid ulcers in the rectosigmoid showed no abnormalities when reexamined by flexible sigmoidoscopy after an interval as short as 7 days (range, 7 to 56 days). Mucosal biopsy specimens from these patients were assessed for apoptosis and epithelial proliferation by determining the MIB-1 labeling index (LI). The LI was increased by 136% after NaP preparation (55 ± 6) compared with biopsy specimens obtained from the same patients during reexamination without NaP preparation (23 ± 6, P = .01). This correlated with the number of apoptotic bodies per 10 colonic crypts (1.2 ± 0.3 v 0.5 ± 0.2, respectively). To determine whether these proliferative changes represent a response to mucosal ulceration, rectosigmoid biopsy specimens were compared in two additional patient groups: an NaP group in whom no gross lesions were evident and a no-NaP group who were not exposed to NaP. Although more modest, similar changes in the LI (42 ± 4 and 30 ± 3, respectively, P = .03) and in the occurrence of apoptotic bodies per 10 colonic crypts (1.3 ± 0.4 and 0.4 ± 0.1, respectively) were observed. We conclude that use of NaP is associated with increased colorectal crypt epithelial cell proliferation. This proliferative response to NaP exposure is evident in the absence of colonoscopically or other histologically recognizable abnormalities. In a proportion of patients, aphthoid ulcers, FAC, or aphthoid lesions serve as markers of mucosal damage by NaP.