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The Turkish Journal of Gastroenterology
2000, Volume 11, No 4, Page(s)
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A fatal complication of sodium-phosphate enema
Egesel Türker1, Sivri Bülent1, Aşık Murat2, Altun Bülent3, Bayraktar Yusuf1
Hacettepe University School of Medicine, Departments of Internal Medicine2 ; Sections of Gastroenterology1 and Nephrology3, Ankara.
Keywords: Fleet enema, hiperfosfatemi, hipernatremi, hipokalsemi.
Summary
A fatal case related to rectal administration of sodium-phosphate (Fleet) enema is presented. A 46-year-old female was admitted to our hospital with hepatic precoma . Following initial eualuation, an enema containing sodium phosphate (Fleet) was administered. This, rather than lactulose enema, was erroneously repeated and resulted in hyperphosphatemia, hypernatremia and hypocalcemia with a fatal outcome. We wish to emphasize the importance of patient selection in the chronic use of hypertonic cathartics such as Fleet enema, which are commonly used bowel cleasing agents.
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  • Summary
  • Introduction
  • Case Presentation
  • Discussion
  • References
  • Introduction
    Sodium-phosphate cathartics have gained popularity in recent years owing to their advantages of small volume, effective bowel cleansing properties and ease of use (1). In many randomized prospective trials they have proved to be safe and well tolerated by patients and also more effective and better tolerated than polyethylene based (Golytely) lavage solutions (1,2). However, an increasing number of reports, mainly in pediatric literature, emphasize the potential risks of these compounds (3-12).We report the case of a patient who was erroneously given six doses of Fleet ene- ma while being treated for hepatic coma and developed adverse effects such as hyperphosphatemia, hypernatremia, hypocalcemia and acidosis.
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  • Summary
  • Introduction
  • Case Presentation
  • Discussion
  • References
  • Case Presentation
    A 46-year-old female was admitted to emergency department in August 1996 with confusion ,diffuse abdominal pain and fever. There was a medical history of two hospitalisations for hepatic encephalopathy and she was under follow-up with the diagnosis of decompensated (due to h B and C viruses) postnecrotic cirrhosis. At her initial evaluation in the emergency room ;she was normotensive ,with a pulse rate of 82,temperature of 38.4 °C and respiratory rate of 24. confused, with flapping tremor, diffuse al tenderness and ascites. Peripheral signs ı sis such as spider nevi, palmar erythema, ren's contracture, white nails and~ pittin were also noted. Laboratory findings were as follows: hemoglobin 9.6 g /dl; hematocrit 26.8 %; WBC 8300 / mm3; pla- telets 79000 / mm3 ; serum sodium 129 mEq / L; potassium 6.6 mEq / L; chloride 109 mEq / L; BUN 87 mg / dl; serum creatinine 2.9 mg / dl; uric acid 7.7 mg / dl; calcium 7.9 mg / dl; phosphate 6.5 mg / dl; ALT 105 U / L; AST 95 U / L; total prote- in 5.5 g /dl; albumin 2.6 g /dl; glucose 78 mg /dl and ammonia 89 UMOL /L ( normal ranges: 11 - 35 ). Diagnostic paracentesis revealed a total cell count of 1600 cells / mm3, leukocytes 1400 mm3, (72 % PNL) and no microorganisms. The patient was admitted to the intensive care unit with a diagnosis of hepatic precoma and spontaneous bacterial peritonitis. She commenced 1 g of cefotaxime i.v. four times daily and standard treatment for hepatic coma. During the first two days of treatment, the patient's clinical picture improved, with the confusion and flapping tremor disappearing. On the third day of therapy, laboratory results from microscopic examination of ascitic fluid proved that the peritonitis treatment was effective (total cell and leukocyte count were decreased). Blood biochemistry results were as follows: sodium 137 mEq / L; potassium 4.1 mEq / L; chloride 107 mEq / L; phosphate 6.0 mg / dl; calcium 8.2 mg / dl; BUN 41 mg / dl; creatinine 1.2 mg / dl; albumin 3.1 g / dl; and ammonia 39 UMOL / L. A gradual decrease in the intensity of hepatic precoma treatment was planned. The following day, her confusion and flapping tremor recurred and after reevaluation of the patient, it was decided to continue the intensive hepatic precoma treatment. Peritoneal infection as an underlying cause of the clinical picture was diagnosed following paracentesis of the ascitic fluid. Urgently drawn blood revealed that sodium was 167 mEq /L; potassium 3.3 mEq /L; calcium 5.5 mg /dl; phosphate 22.7 mg /dl; blood pH was 7,21. Urinary sodium was 8.1 mmol /L while urine output decreased to 15 ml / hour. Electrocardiog- raphy showed Q-T interval prolongation and mul- tifocal premature atrial beats. The patient was assessed by the Nephrology Department and the treatment protocol was reevaluated. After close in- vestigation, it was found that the nurses had erroneously administered Fleet rather than lactulose enemas during the previous 30 hours (a total of six enemas, 133 mls each) Fleet enemas were immediately discontinued and lactulose enemas commenced. Laboratory findings three hours later we- re as follows: sodium 178 mEq / 1; potassium 3.1 mEq / 1; chloride 138 mEq / 1; phosphate, 24.3 mg / dl; calcium, 5.1 mg / dl. An emergency hemodialy- sis was planned, but the patient was found to be unsuitable for hemodialysis due to severe hypo- tension which was resistant to vasopressor agents. The patient then had a cardiac arrest which did not respond to resuscitation measures.
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  • Summary
  • Introduction
  • Case Presentation
  • Discussion
  • References
  • Discussion
    Sodium-phosphate compounds are commonly used bowel cleansing agents, either as enemas or oral preparations. For colon cleansing in particular, a single oral dose of 90 ml (Fleet) phospho-soda has been found to be safe and efI'ective (1). Small volu- me and . easy administration are advantages of Fleet enema (1,2), particularly in relationship to patient tolerance. However, there are many reports about the risks of these compounds, especi- ally in the pediatric age group. These untoward ef fects are hypernatremia, hyperphosphatemia, hypocalcemia, acidosis, cardiac arrest and death (3-12). Such ctimplications are also more readily seen in renal failure, cardiac failure and patients who have massive ascites (1,10,12).

    Wilberg et al.ı3 administered a phosphate containing oral laxative at a dose of 7 g elemental phosphorus to normal subjects prior to barium enema. This study resulted in an increase in serum phosphorus from a mean control value of 3.4 mg / dl to a peak of 6.9 mg / dl after three hours and a decline in serum calcium in all subjects. Another study with 90 mls phospho-soda (containing 11.5 g elemental phosphorus) did not yield any significant decrease in serum calcium levels, despite a signifıcant increase in phosphorus (7.2 ± 0.6 mg / dl)1. In Cohan's study,14 two applications of Fleet phospho-soda enema were used and an increased serum phosphorus concentration was detected without any other electrolyte abnormalities. The case presented here was found to have hyperphosphatemia, hypernatremia, hypocalcemia and acidosis. At the time of this acute illness, a dilutional hyponatremia was noted. Later, an increase of sodium to 178 mEq / L despite massive ascites and hypernatremia was striking. It was thought that the patient had prerenal azotemia and that concomitant increased absorption of sodium from the gut lumen added to this increased sodium level. In fact, the hyperphosphatemia was related to the inappropriate use of Fleet enema. Hypocalcemia was probably due to extraosseous deposition of calcium phosphate12,15. Unfortunately, the patient was erroneously given six doses of 133 ml Fleet enema, containing 19 g of monobasic sodium-phosphate and 7 g of dibasic sodium- phosphate. The negative impact of Fleet enema usage in this particular patient may be summarized as follows:
    (1) She had prerenal azotemia;
    (2) Fleet enema was used in excess of drug safety limits;
    (3) The patient had massive ascites and hepatic failure. It is concluded that sodium phosphate compounds should be used in recommended dosages only in selected patient groups. Patients should be evaluated carefully for any underlying disease and particular care should be taken in patients with intestinal obstruction, motility problems, advanced heart failure, renal failure, hepatic failure and asci- tes. As was learned from this particular case, diagnosis of such fatal.complications is difficult and even if no underlying disease exists, patients should be closely monitored for serum electrolytes.
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  • Summary
  • Introduction
  • Case Presentation
  • Discussion
  • References
  • References

    1) .Van

    2) .Cohen SM, Wexner SD, Binderow SR, et al. Prospective, randomized, endoacopic-blinded trial comparing precolonoscopy bowel cleansing methods. Dis Colon Rectum 1994; 37: 689-96.

    3) .Davis RF, Eichner JM, Bleyer WA, et al. Hypocalcemia hyperphosphatemia, and dehydration following a single hypertonic phosphate enema. J Pediatr 1977; 90: 484-5.

    4) .Reedy JC, Zwiren GT. Enema-induced hypocalcemia and hyperphosphatemia leading to cardiac arrest during induction of anesthesia in an outpatient surgery center. Anesthesiology 1983; 59: 578-9.

    5) .Martin RR, Lisehora GR, Braxton M, et al. Fatal poisoning from sodium phosphate enema: A case report and experi- mental etudy. JAMA 1987; 257: 2190-2.

    6) .Fonkalsrud EW, Keen J. Hypernatremia dehydration from hypertonic enemas in congenital megacolon. JAMA 1967; 199: 584-6.

    7) .Connel TH. Fatal hypocalcemia from phosphate absorption from laxative preparations. JAMA 1971; 216: 147-8.

    8) .Biberstein M, Parker BA. Enema-induced hyperphospha- temia. Am J Med 1985; 79: 645-6.

    9) .Korzets A, Dicker D, Chaimoff C, et al. Lifethreatening hyperphosphatemia and hypocalcemic tetany following the use of Fleet enemas. J Am Geriatr Soc 1992; 40: 620-1.

    10) .Zisper RD, Bischel MD, Abrams DE. Hypocalcemic tetany due to sodium phosphate ingestion in acute renal failure. Nephron 1975; 14: 378-81.

    11) . Haskell LP. Hypocalcemic tetany induced by hypertonic- phoaphate enema. Lancet 1985; 2: 1433.

    12) .Fas1s R, Do S, Hixson LJ. Fatal Hyperphosphatemia folla wing Fleet phospo-soda in a patient with colonic ileus. Am J Gastroenterol 1993; 88: 929-32.

    13) .Wiberg JJ, Tııxzıer GG, Nuttall FQ. Effect of phosphate or magnesium cathartica on serum calcium: Obaervations in normocalcemic patienta. Arch Intern Med 1978; 138: 114- 6.

    14) .Cohan CF, Kadakia SC, Kadakia AS. Serum electrolyte, mineral and blood pH changea after phoaphate enema, water enema and electrolyte lavage solution enema for fle~ble sigmoidoscopy. Gastrointest Endosc 1992; 38: 575-8.

    15) .Yu GC, Lee DB. Clinical disordera of phosphorus metabo- lism. Weat J Med 1987; 147: 569-7.

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  • Summary
  • Introduction
  • Case Presentation
  • Discussion
  • References
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