Severe hyperphosphoremia and hypernatremia induced by sodium phosphate enemas

García Chumillas, Vanesa; Borrego García, Elena; González Martínez, Miguel Ángel

doi:10.1016/j.medcle.2023.06.040

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It consists of electrolyte replacement, withdrawal of potentiating drugs and placement of nasogastric and rectal tube with cleansing enemas; colonic decompression is used in the most severe cases.<a class="elsevierStyleCrossRef" href="#bib0005">1</a>The use of enemas, particularly sodium phosphate enemas, is often associated with electrolyte disturbances and calcium-phosphorus metabolism disorders, which are usually self-limiting, but can be severe in the presence of diseases that increase phosphate absorption, such as inflammatory bowel disease, or hinder its elimination, such as renal failure or paralytic ileus.<a class="elsevierStyleCrossRefs" href="#bib0010">2,3</a>The following is a case of an Ogilvie syndrome secondary to cytomegalovirus infection whose intensive treatment with sodium phosphate enemas caused severe dyselectrolytemia with secondary cardiopulmonary arrest (CPA).A 71-year-old male patient with a 48 h history of abdominal distension, constipation and vomiting. An abdominal CT scan was performed, showing colonic dilatation compatible with Ogilvie syndrome. Decompressive colonoscopy was performed after a nasogastric and rectal tube with sodium phosphate enemas did not produce any response. The course was unfavourable and constipation persisted despite enemas. On the second day of hospitalisation, the patient had CPA, resuscitated satisfactorily, requiring haemodynamic stabilisation in the ICU. A pre-CPA blood test showed: urea 45 (18–37.7) mg/dl; creatinine 1 (0.67–1.17) mg/dl; sodium 173 (136–145) mEq/l; potassium 2.2 (3.5–5.1) mEq/l; calcium 6.8 (8.8–10.6) mg/dl; phosphorus >20 (2.5–4.5) mg/dl; magnesium 2.4 (1.6–2.6) mg/dl and parathyroid hormone 400 (12–110) pg/ml. No significant findings in other parameters. Immediate electrolyte replacement therapy was started with 10% calcium gluconate, potassium chloride, loop diuretics, free water and phosphorus chelators via nasogastric tube; enemas were discontinued. Maintained diuresis rate >100 ml/h. A 24 h urinalysis showed: sodium 131 (20–110) mEq/l; potassium 30 (40–136) mEq/l; calcium 3.7 (7–24) mg/dl; phosphorus 207.5 (40–136) mg/dl and magnesium 4.97 (4.1–13.8) mg/dl. After medical treatment, he showed gradual recovery of clinical and haemodynamic status and laboratory parameters returned to normal levels. From a gastrointestinal perspective, a new decompressive colonoscopy was performed with a positive result for cytomegalovirus. Treatment was started with oral valganciclovir, intravenous neostigmine, and later oral cinitapride, with improvement of the symptoms.The use of sodium phosphate enemas can sometimes cause severe toxicity. The main alterations they cause are hyperphosphataemia, hypocalcaemia and hypernatraemia. This is due to the high concentration of sodium and phosphorus in these preparations, which generates colonic hyperosmolarity causing water to pass into the intestinal lumen as it is exchanged for sodium and causing hypernatraemic dehydration. Phosphorus is excreted via the kidneys and absorbed mainly in the jejunum, favoured by vitamin D4, binding to ionic calcium and forming calcium phosphate which precipitates in tissues, causing a compensatory increase in parathyroid hormone.Severe hyperphosphataemia with fatal outcome has been reported in predisposed patients with renal insufficiency or intestinal transit disorders, although it can also occur in patients without predisposing risk factors.<a class="elsevierStyleCrossRefs" href="#bib0010">2,4</a>Hyperphosphatemia toxicity is determined by the resulting hypocalcaemia, which can cause neuromuscular (tetany, convulsions and coma) and haemodynamic (hypotension, arrhythmias and decreased cardiac contractility) symptoms; as occurred in our case with a CPA outcome.<a class="elsevierStyleCrossRef" href="#bib0015">3</a>Its early treatment is of vital importance and is based on promoting renal phosphorus excretion through intensive fluid therapy and diuretics, although these should be used with caution as they may accentuate hypocalcaemia. Oral phosphate chelating agents, such as aluminium hydroxide, have been shown to be effective as an adjuvant treatment in acute hyperphosphataemia.<a class="elsevierStyleCrossRef" href="#bib0025">5</a> Urgent dialysis will also be necessary in cases of renal failure or refractory to treatment. Moreover, correction of the associated hypocalcaemia is recommended only in cases of severe symptoms, as it favours the development of calcifications.<a class="elsevierStyleCrossRef" href="#bib0020">4</a>The causality algorithm of the Spanish Pharmacovigilance System (SEFV) was applied and the adverse reaction secondary to enemas was confirmed as definitive, with a score of +8, as there was an evident temporal sequence between administration and the onset of clinical symptoms, previous knowledge in the literature, the presence of predisposing factors (Ogilvie syndrome), as well as complete resolution and no recurrence of the symptoms on discontinuation of the exposure.We consider the case described to be relevant in view of the need to raise awareness of the potential side effects related to these agents, avoiding their indiscriminate administration and discouraging their use in patients with predisposing risk factors.Ethical considerationsThe authors declare that they have followed the protocols established in their work centre to access the patient's medical record data in order to be able to make this publication available to the scientific community.FundingThe authors have not received funding for this article." 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Rockey" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:3 [ "tituloSerie" => "Medicine (Baltimore)" "fecha" => "2018" "volumen" => "97" ] ] ] ] ] ] 1 => array:3 [ "identificador" => "bib0010" "etiqueta" => "2" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Extreme hyperphosphatemia and hypocalcemic coma associated with phosphate enema" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:2 [ 0 => "H.J. Hsu" 1 => "M.S. Wu" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.2169/internalmedicine.47.0704" "Revista" => array:6 [ "tituloSerie" => "Intern Med" "fecha" => "2008" "volumen" => "47" "paginaInicial" => "643" "paginaFinal" => "646" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/18379152" "web" => "Medline" ] ] ] ] ] ] ] ] 2 => array:3 [ "identificador" => "bib0015" "etiqueta" => "3" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Hiperfosforemia e hipolcacemia grave tras la administración de un enema de fosfato sódico" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:4 [ 0 => "G. Oñoro" 1 => "G. de Lama" 2 => "A. Pérez-Martínez" 3 => "M. González-Vicent" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1016/j.medin.2013.01.011" "Revista" => array:6 [ "tituloSerie" => "Med Intensiva" "fecha" => "2014" "volumen" => "38" "paginaInicial" => "263" "paginaFinal" => "264" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/23890987" "web" => "Medline" ] ] ] ] ] ] ] ] 3 => array:3 [ "identificador" => "bib0020" "etiqueta" => "4" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Enema-induced severe hyperphosphatemia in children" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:3 [ 0 => "A. Biebl" 1 => "A. Grillenberger" 2 => "K. Schmitt" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1007/s00431-008-0705-2" "Revista" => array:6 [ "tituloSerie" => "Eur J Pediatr" "fecha" => "2009" "volumen" => "168" "paginaInicial" => "111" "paginaFinal" => "112" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/18408952" "web" => "Medline" ] ] ] ] ] ] ] ] 4 => array:3 [ "identificador" => "bib0025" "etiqueta" => "5" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Oral phosphate binders" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:1 [ 0 => "A.J. Hutchison" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1038/ki.2009.60" "Revista" => array:6 [ "tituloSerie" => "Kidney Int" "fecha" => "2009" "volumen" => "75" "paginaInicial" => "906" "paginaFinal" => "914" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/19279554" "web" => "Medline" ] ] ] ] ] ] ] ] ] ] ] ] ] "idiomaDefecto" => "en" "url" => "/23870206/0000016100000012/v2_202401260944/S2387020623004941/v2_202401260944/en/main.assets" "Apartado" => array:4 [ "identificador" => "43309" "tipo" => "SECCION" "en" => array:2 [ "titulo" => "Letters to the Editor" "idiomaDefecto" => true ] "idiomaDefecto" => "en" ] "PDF" => "https://static.elsevier.es/multimedia/23870206/0000016100000012/v2_202401260944/S2387020623004941/v2_202401260944/en/main.pdf?idApp=UINPBA00004N&text.app=https://www.elsevier.es/" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2387020623004941?idApp=UINPBA00004N"]

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Vol. 161. Issue 12.