Related Experiment Video

Updated: Aug 4, 2026

The Hypoxic Ischemic Encephalopathy Model of Perinatal Ischemia
08:47

The Hypoxic Ischemic Encephalopathy Model of Perinatal Ischemia

Published on: November 19, 2008

Recovery of metabolic acidosis in term infants with postasphyxial hypoxic-ischemic encephalopathy

P S Shah1, N V Raju, J Beyene

  • 1Division of Neonatology, The Hospital for Sick Children, Toronto, Canada.

Acta Paediatrica (Oslo, Norway : 1992)
|September 2, 2003
PubMed

Insights

Base deficit (BD) in infants with hypoxic ischemic encephalopathy normalizes within 4 hours of birth. Recovery rates of BD were similar between infants with good and adverse outcomes, regardless of asphyxia patterns.

Area of Science:

  • Neonatalogy
  • Pediatric Critical Care
  • Biochemistry

Background:

  • Hypoxic ischemic encephalopathy (HIE) is a serious condition in newborns due to birth asphyxia.
  • Base deficit (BD) is a key indicator of metabolic acidosis in HIE.
  • Understanding BD recovery patterns is crucial for predicting outcomes.

Purpose of the Study:

  • To characterize base deficit (BD) values and postnatal recovery rates in infants with HIE.
  • To investigate the relationship between BD recovery rate, severe adverse outcomes, and asphyxia timing.

Main Methods:

  • Collected neonatal clinical and laboratory data (n=244) and long-term outcome data (n=218).
  • Analyzed BD recovery rates in 60-minute intervals post-birth.
  • Compared recovery rates between outcome groups using generalized estimating equations.

Main Results:

  • Base deficit normalized within 4 hours for most infants (235/244).
  • BD recovery rates were similar for infants with good vs. severe adverse outcomes (0.11 vs. 0.09 mmol/l/min).
  • Recovery rates were consistent regardless of buffer therapy or asphyxia pattern (acute total vs. prolonged partial).

Conclusions:

  • The majority of infants with severe intrapartum asphyxia achieve normal base deficit levels within 4 hours.
  • Base deficit recovery rates do not differentiate between good and adverse outcomes in HIE.
  • Asphyxia timing patterns do not influence base deficit recovery profiles.
Abstract

More Related Videos

A Piglet Model of Neonatal Hypoxic-Ischemic Encephalopathy10:30

A Piglet Model of Neonatal Hypoxic-Ischemic Encephalopathy

Published on: May 16, 2015

A Piglet Perinatal Asphyxia Model to Study Cardiac Injury and Hemodynamics after Cardiac Arrest, Resuscitation, and the Return of Spontaneous Circulation10:55

A Piglet Perinatal Asphyxia Model to Study Cardiac Injury and Hemodynamics after Cardiac Arrest, Resuscitation, and the Return of Spontaneous Circulation

Published on: January 13, 2023

Related Concept Videos

Diagnosing Acidosis and Alkalosis01:24

Diagnosing Acidosis and Alkalosis

Diagnosing acid-base imbalances involves systematically analyzing arterial blood samples, focusing on three key measurements: pH, bicarbonate (HCO3−) concentration, and carbon dioxide partial pressure (PCO2). This analysis follows a four-step process that helps identify the imbalance's underlying cause and nature.
First, the pH level is assessed to determine whether the blood pH is normal (7.35–7.45), low (acidosis), or high (alkalosis).
Next, the PCO2  and HCO3−  values are examined to...
Acute Respiratory Failure-II01:21

Acute Respiratory Failure-II

Type I Respiratory Failure, or hypoxemic respiratory failure, occurs when the partial pressure of oxygen (PaO2) in arterial blood falls below 60 mmHg while breathing room air without a corresponding increase in arterial carbon dioxide levels (PaCO2). This condition highlights a significant impairment in the lungs' capacity to oxygenate the blood.
The underlying physiological abnormalities that contribute to hypoxemic respiratory failure include:
Acute Respiratory Failure-III01:30

Acute Respiratory Failure-III

Hypercapnic respiratory failure, also known as Type 2 or ventilatory respiratory failure, is a severe condition characterized by the body's inability to effectively remove carbon dioxide (CO2) from the bloodstream. It leads to an arterial CO2 pressure (PaCO2) exceeding 45 mmHg and a blood pH above 7.35. This situation indicates that the body's ventilatory demand, or the ventilation needed to maintain normal PaCO2 levels, surpasses its supply or the maximum gas flow achievable without causing...
Acute Respiratory Failure-V01:29

Acute Respiratory Failure-V

The treatment for acute respiratory failure varies based on factors like the underlying cause, overall health, and severity. A collaborative healthcare team is essential for early detection, often through arterial blood gas analysis. Identifying the cause is the primary goal, with treatment strategies adjusted for ventilation/perfusion (V/Q) mismatch, shunting, or diffusion impairment.
Ensure that patients are monitored continuously for their response to therapy, including changes in...
Diabetic Ketoacidosis l: Introduction01:25

Diabetic Ketoacidosis l: Introduction

DefinitionDiabetic ketoacidosis (DKA) is an acute, life-threatening complication of diabetes mellitus, characterized by a triad of hyperglycemia (blood glucose >250 mg/dL), ketonemia or ketonuria, and metabolic acidosis (arterial pH <7.30 and serum bicarbonate <18 mEq/L). It results from insulin deficiency combined with elevated levels of counterregulatory hormones—glucagon, catecholamines, cortisol, and growth hormone—leading to increased lipolysis, hepatic ketone production, and...
Diabetic Ketoacidosis ll: Pathophysiology01:22

Diabetic Ketoacidosis ll: Pathophysiology

Diabetic ketoacidosis (DKA) is a metabolic emergency characterized by hyperglycemia, ketonemia, and metabolic acidosis. It results from severe insulin deficiency and an excess of counterregulatory hormones, leading to uncontrolled lipolysis, ketogenesis, and widespread electrolyte and fluid disturbances.Pathophysiology The central event in DKA is a profound loss of insulin action. Without insulin, glucose uptake in insulin-dependent tissues is impaired, while hepatic glucose production...