Aetiological diagnosis of hyponatraemia in non-critical patients on total parenteral nutrition: A prospective multicentre study.

Aetiology of hyponatraemia Estímulo fisiológico de la secreción de AVP Etiología de la hiponatremia Nutrición parenteral Parenteral nutrition Physiological stimuli of AVP secretion SIADH

Journal

Endocrinologia, diabetes y nutricion
ISSN: 2530-0180
Titre abrégé: Endocrinol Diabetes Nutr (Engl Ed)
Pays: Spain
ID NLM: 101717565

Informations de publication

Date de publication:
06 Jul 2021
Historique:
received: 23 11 2020
revised: 11 02 2021
accepted: 15 02 2021
entrez: 10 7 2021
pubmed: 11 7 2021
medline: 11 7 2021
Statut: aheadofprint

Résumé

In patients receiving total parenteral nutrition (TPN), the frequency of hyponatraemia is high. However, the causes of hyponatraemia in TPN have not been elucidated, although diagnosis is required for appropriate therapy. The aim of this study is to describe the aetiology of hyponatraemia in non-critical hospitalised patients receiving TPN. Prospective multicentre study in 19 Spanish hospitals. Non-critically hyponatraemic patients receiving TPN and presenting hyponatraemia over a 9-month period were studied. Data collected included sex, age, previous comorbidities, and serum sodium levels (SNa) before and following TPN initiation. Parameters for study of hyponatraemia were also included: clinical volaemia, the presence of pain, nausea, gastrointestinal losses, diuretic use, oedema, renal function, plasma and urine osmolality, urinary electrolytes, cortisolaemia, and thyroid stimulating hormone. 162 patients were included, 53.7% males, age 66.4 (SD13.8) years. Volume status was evaluated in 142 (88%): 21 (14.8%) were hypovolaemic, 96 (67.6%) euvolaemic and 25 (17.6%) hypervolaemic. In 111/142 patients the analytical assessment of hyponatraemia was completed. Hypovolaemic hyponatraemia was secondary to GI losses in 10/111 (9%), and to diuretics in 3/111 (2.7%). Euvolaemic hyponatraemia was due to Syndrome of Inappropriate Antidiuretic Hormone secretion (SIADH) in 47/111 (42.4%), and to physiological stimuli of Arginine Vasopressin (AVP) secretion in 28/111 (25.2%). Hypervolaemic hyponatraemia was induced by heart failure in 19/111 (17.1%), cirrhosis of the liver in 4/111 (3.6%). SIADH was the most frequent cause of hyponatraemia in patients receiving TPN. The second most frequent cause was physiological stimuli of AVP secretion induced by pain/nausea.

Sections du résumé

BACKGROUND BACKGROUND
In patients receiving total parenteral nutrition (TPN), the frequency of hyponatraemia is high. However, the causes of hyponatraemia in TPN have not been elucidated, although diagnosis is required for appropriate therapy. The aim of this study is to describe the aetiology of hyponatraemia in non-critical hospitalised patients receiving TPN.
METHODS METHODS
Prospective multicentre study in 19 Spanish hospitals. Non-critically hyponatraemic patients receiving TPN and presenting hyponatraemia over a 9-month period were studied. Data collected included sex, age, previous comorbidities, and serum sodium levels (SNa) before and following TPN initiation. Parameters for study of hyponatraemia were also included: clinical volaemia, the presence of pain, nausea, gastrointestinal losses, diuretic use, oedema, renal function, plasma and urine osmolality, urinary electrolytes, cortisolaemia, and thyroid stimulating hormone.
RESULTS RESULTS
162 patients were included, 53.7% males, age 66.4 (SD13.8) years. Volume status was evaluated in 142 (88%): 21 (14.8%) were hypovolaemic, 96 (67.6%) euvolaemic and 25 (17.6%) hypervolaemic. In 111/142 patients the analytical assessment of hyponatraemia was completed. Hypovolaemic hyponatraemia was secondary to GI losses in 10/111 (9%), and to diuretics in 3/111 (2.7%). Euvolaemic hyponatraemia was due to Syndrome of Inappropriate Antidiuretic Hormone secretion (SIADH) in 47/111 (42.4%), and to physiological stimuli of Arginine Vasopressin (AVP) secretion in 28/111 (25.2%). Hypervolaemic hyponatraemia was induced by heart failure in 19/111 (17.1%), cirrhosis of the liver in 4/111 (3.6%).
CONCLUSIONS CONCLUSIONS
SIADH was the most frequent cause of hyponatraemia in patients receiving TPN. The second most frequent cause was physiological stimuli of AVP secretion induced by pain/nausea.

Identifiants

pubmed: 34244097
pii: S2530-0164(21)00123-3
doi: 10.1016/j.endinu.2021.02.006
pii:
doi:

Types de publication

Journal Article

Langues

eng spa

Informations de copyright

Copyright © 2021 SEEN y SED. Publicado por Elsevier España, S.L.U. All rights reserved.

Auteurs

Ana Ortolá Buigues (A)

Endocrinology and Nutrition Department, Hospital Clínico Universitario de Valladolid and Centro de Investigación de Endocrinología y Nutrición (IEN), Universidad de Valladolid, Valladolid, Spain. Electronic address: anaortola@hotmail.com.

Emilia Gómez-Hoyos (E)

Endocrinology and Nutrition Department, Hospital Clínico Universitario de Valladolid and Centro de Investigación de Endocrinología y Nutrición (IEN), Universidad de Valladolid, Valladolid, Spain.

María Dolores Ballesteros Pomar (MD)

Endocrinology and Nutrition Department, Complejo Asistencial Universitario de León, León, Spain.

Alfonso Vidal Casariego (A)

Endocrinology and Nutrition Department, Complejo Asistencial Universitario de León, León, Spain.

Yaiza García Delgado (Y)

Endocrinology and Nutrition Department, Hospital Universitario Insular, Las Palmas de Gran Canaria, Spain.

María Julia Ocón Bretón (MJ)

Endocrinology and Nutrition Department, Hospital Clínico Universitario Lozano Blesa, Zaragoza, Spain.

Ángel Luis Abad González (ÁL)

Endocrinology and Nutrition Department, Hospital General Universitario de Alicante, Alicante, Spain.

Luis Miguel Luengo Pérez (LM)

Endocrinology and Nutrition Department, Hospital Universitario Infanta Cristina, Badajoz, Spain.

Pilar Matía Martín (P)

Endocrinology and Nutrition Department, Hospital Clínico Universitario San Carlos and Instituto de Investigación Sanitaria San Carlos (IDISSC), Madrid, Spain.

María José Tapia Guerrero (MJ)

Endocrinology and Nutrition Department, Hospital Regional Universitario de Málaga, Málaga, Spain.

María Dolores Del Olmo García (MD)

Endocrinology and Nutrition Department, Hospital Universitario Severo Ochoa, Leganés, Spain.

Ana Herrero Ruiz (A)

Endocrinology and Nutrition Department, Hospital Clínico Universitario de Salamanca, Salamanca, Spain.

Julia Álvarez Hernández (J)

Endocrinology and Nutrition Department, Hospital Universitario Príncipe de Asturias, Getafe, Spain.

Cristina Tejera Pérez (C)

Endocrinology and Nutrition Department, Complejo Hospitalario Universitario de Ferrol, Ferrol, Spain.

Alejandra Herranz Antolín (A)

Endocrinology and Nutrition Department, Hospital Universitario de Guadalajara, Guadalajara, Spain.

Carmen Tenorio Jiménez (C)

Endocrinology and Nutrition Department, Complejo Hospitalario de Jaén, Jaén, Spain.

María Victoria García Zafra (MV)

Endocrinology and Nutrition Department, Hospital General Universitario Santa Lucía, Cartagena, Spain.

Francisco Botella Romero (F)

Endocrinology and Nutrition Department, Complejo Hospitalario Universitario de Albacete, Albacete, Spain.

María Argente Pla (M)

Endocrinology and Nutrition Department, Hospital Universitario y Politécnico de La Fe, Valencia, Spain.

Miguel Ángel Martínez Olmos (MÁ)

Endocrinology and Nutrition Department, Complejo Hospitalario Universitario de Santiago, Santiago de Compostela, Spain.

Irene Bretón Lemes (I)

Endocrinology and Nutrition Department, Hospital Universitario Gregorio Marañón, Madrid, Spain.

Isabelle Runkle De la Vega (I)

Endocrinology and Nutrition Department, Hospital Clínico Universitario San Carlos and Instituto de Investigación Sanitaria San Carlos (IDISSC), Madrid, Spain.

Daniel De Luis Román (D)

Endocrinology and Nutrition Department, Hospital Clínico Universitario de Valladolid and Centro de Investigación de Endocrinología y Nutrición (IEN), Universidad de Valladolid, Valladolid, Spain.

Classifications MeSH