Home
About Us
Issues
Authors
Reviewers
Users
Subscription
Our Other Journals
Neonatal Database
Neonatal Database Download
Neonatal Journal Abstracts
Feedback
Salient Features
Open Access
Editorial Board
Publisher
Publication Ethics & Malpractice
Journal Policy
Peer Review Process
Contact Us
Current Issue
Forthcoming
Article Archive
Access Statistics
Simple Search
Advanced Search
Submit an Article
Instructions
Assistance
Publication Fee
Paid Services
Apply As Reviewer
Acknowledgment
Register Here
Register For Article Submission
Login Here
Login For Article Submission
Annual
Buy One Issue
Payment Options
How to Order
JCDR
IJARS
NJLM

 

Welcome : Guest

Users Online :

 

 

 

 

 

 

 

 

Original article / research

Year :2013 Month : April Volume : 1 Issue : 1 Page : 8 - 17

Pathogenesis of Metabolic Acidosis in Preterm Infants

 
Correspondence Address :
Christopher Geoffrey Alexander Aikenay,
C G A Aiken,
729 Frankley Road, New Plymouth 4371,
New Zealand.
Phone: +64 6 753 2950
Email: geoffaiken@xtra.co.nz
Objective: To determine how the balance between mineral base, and carbonic and organic acids is altered to cause metabolic acidosis in preterm infants. Study Design: Mineral balance and arterial blood measurements of 3 groups of preterm infants given 5 different total parenteral nutrition (TPN) regimens were analyzed. Mineral base was measured as the difference between mineral cations and anions. Organic acid was measured as the difference between mineral base, bicarbonate and protein anion. Results: The degree of metabolic acidosis measured as base excess, was determined by deviation in both mineral base and organic acid from normal. Sodium minus chloride balance determined change in arterial blood mineral base. TPN containing more chloride than sodium caused mineral acidosis with low mineral base, whereas TPN containing more sodium than chloride caused mineral alkalosis with high mineral base. Lactic, organic and carbonic acidosis all increased mineral base. Arterial blood organic acid was determined by: 1. Glomerular filtration rate: Low rates after delivery caused high organic acid that fell as GFR improved. 2. TPN non metabolized organic acid content: Gluconate and sulphate caused organic acidosis by accumulating in blood and mineral acidosis by urine excretion resulting in mineral base loss. 3. Rate of protein catabolism: Increased protein catabolism from TPN providing only 25 kcal/g amino acids or from dexamethasone caused organic acidosis. Conclusion: Metabolic acidosis was caused by high organic acid, resulting from low glomerular filtration rates in the first 1-2 weeks, exacerbated by TPN containing gluconate or sulphate or only 25 kcal/g amino acids. Renal bicarbonate wasting could not account for metabolic acidosis.
 
[ FULL TEXT ]   |   [ ]
 

Article Utilities

  • Readers Comments
  • Article in PDF
  • Citation Manager
  • Article Statistics
  • Link to PUBMED
  • Print this Article
  • Send to a Friend

Quick Links

REVIEWER
ACCESS STATISTICS
Home  |  About Us  |  Online First  |  Current Issue  |  Simple Search  |  Advance Search  |  Register  |  Login  |  Contact  | 
IJNMR Pre-Publishing  |  Reviewer  |  Articles Archive  |  Access Statistics
© 2023 INDIAN JOURNAL OF NEONATAL MEDICINE & RESEARCH (IJNMR), ISSN : 2277-8527.
EDITORIAL OFFICE : 3rd Floor, Hemraj Jain Building, 4352 Pahari Dhiraj, Delhi, India 110006,Phone : 01123848553

* This Journal is owned and run by medical professionals *