NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-.

Cover of StatPearls

StatPearls [Internet].

Show details

Birth Asphyxia

; .

Author Information

Last Update: August 30, 2020.

Continuing Education Activity

Perinatal asphyxia is a lack of blood flow or gas exchange to or from the fetus in the period immediately before, during, or after the birth process. Perinatal asphyxia can result in profound systemic and neurologic sequelae due decreased blood flow and/or oxygen to a fetus or infant during the peripartum period. When placental (prenatal) or pulmonary (immediate post-natal) gas exchange is compromised or ceases altogether, there is partial (hypoxia) or complete (anoxia) lack of oxygen to the vital organs. This results in progressive hypoxemia and hypercapnia. If the hypoxemia is severe enough, the tissues and vital organs (muscle, liver, heart, and ultimately the brain) will develop an oxygen debt. Anaerobic glycolysis and lactic acidosis will result. Neonatal hypoxic-ischemic encephalopathy refers specifically to the neurologic sequelae of perinatal asphyxia. This activity reviews the causes of birth asphyxia, its pathophysiology and highlights the role of the interprofessional team in its management.

Objectives:

  • Identify the etiology of birth asphyxia.
  • Review the presentation of a patient with birth asphyxia.
  • Outline the treatment and management options available for birth asphyxia.
  • Explain interprofessional team strategies for improving care and outcomes in patients with birth asphyxia.
Access free multiple choice questions on this topic.

Introduction

Perinatal asphyxia is a lack of blood flow or gas exchange to or from the fetus in the period immediately before, during, or after the birth process. Perinatal asphyxia can result in profound systemic and neurologic sequelae due decreased blood flow and/or oxygen to a fetus or infant during the peripartum period. When placental (prenatal) or pulmonary (immediate post-natal) gas exchange is compromised or ceases altogether, there is partial (hypoxia) or complete (anoxia) lack of oxygen to the vital organs. This results in progressive hypoxemia and hypercapnia. If the hypoxemia is severe enough, the tissues and vital organs (muscle, liver, heart, and ultimately the brain) will develop an oxygen debt. Anaerobic glycolysis and lactic acidosis will result.  Neonatal hypoxic-ischemic encephalopathy refers specifically to the neurologic sequelae of perinatal asphyxia.[1][2]

The diagnostic criteria for neonatal hypoxic-ischemic encephalopathy are as follows:

  • Metabolic acidosis with pH <7.0 (in umbilical cord or infant blood sample)
  • Base Deficit -12
  • APGAR score = five at 10 minutes with a continued need for resuscitation
  • Presence of multiple organ-system failures
  • Clinical evidence of encephalopathy:  hypotonia, abnormal oculomotor or pupillary movements, weak or absent suck, apnea, hyperpnea, or clinical seizures
  • Neurologic findings cannot be attributed to other cause (inborn error of metabolism, a genetic disorder, congenital neurologic disorder, medication effect)

Etiology

Perinatal asphyxia can occur due to maternal hemodynamic compromise (amniotic fluid embolus), uterine conditions (uterine rupture), or placenta and umbilical cord (placental abruption, umbilical cord knot or compression) and infection. The asphyxia can occur prior to the birth or can occur immediately following birth in a compromised patient requiring resuscitation.[3][4][5]

The majority of cases of perinatal asphyxia occur intrapartum, although 20% occur antepartum and other cases occur in the early post-natal period. Perinatal asphyxia can occur due to maternal events (hemorrhage, amniotic fluid embolism; hemodynamic collapse), placental events (acute abruption), uterine events (rupture), cord events (tight nuchal cord, cord prolapse/avulsion) and intrapartum infection (maternal fever in labor). A careful obstetrical and peripartum history is essential to determine the etiology.

Epidemiology

The incidence of perinatal asphyxia is two per 1000 births in developed countries, but the rate is up to 10 times higher in developing countries where there may be limited access to maternal and neonatal care. Of those infants affected, 15-20% die in the neonatal period, and up to 25% of survivors are left with permanent neurologic deficits.[6]

Pathophysiology

There are three stages to brain injury in hypoxic-ischemic encephalopathy. First, there is an immediate primary neuronal injury that occurs due to interruption of oxygen and glucose to the brain. This decreases ATP and results in failure of the ATP-dependent NaK pump. Sodium enters the cell followed by water, causing cell swelling, widespread depolarization, and cell death. Cell death and lysis cause release of glutamate, an excitatory amino acid, which causes an increase in intracellular calcium and further cell death.

Following the immediate injury is a latent period of about six hours, during which reperfusion occurs, and some cells recover.

Late secondary neuronal injury occurs over the next 24-48 hours as reperfusion results in blood flow to and from damaged areas, spreading toxic neurotransmitters and widening the area of brain affected.

History and Physical

Perinatal asphyxia can result in systemic effects, including neurologic insult, respiratory distress and pulmonary hypertension, and liver, myocardial, and renal dysfunction. Depending on the severity and timing of the hypoxic insult, a neonate with hypoxic-ischemic encephalopathy due to perinatal asphyxia can demonstrate a variety of neurologic findings. Using the Sarnat staging for encephalopathy can be useful. In Sarnat Stage I, the least severe stage, there is generalized sympathetic tone and the neonate may be hyper-alert with prolonged periods of wakefulness, mydriasis and increased deep tendon reflexes. In Sarnat Stage II, the neonate may be lethargic or obtunded, with decreased tone, strong distal flexion, and generalized parasympathetic tone with miosis, bradycardia and increased secretions. Seizures are common in Sarnat Stage II. Sarnat Stage III, the most severe, is characterized by a profoundly decreased level of consciousness, flaccid tone, decreased deep tendon reflexes and very abnormal EEG. Clinical seizures are less common in Sarnat Stage III due to the profound injury in the brain preventing the propagation of clinical seizures.

Evaluation

A chest radiograph may determine the need for intubation and/or need for exogenous surfactant therapy. An arterial blood gas is useful in diagnosing respiratory versus metabolic acidosis and degree of hypoxemia. Liver damage can be determined by serum transaminase levels and coagulation factors. Troponin and CK-MB can be useful in determining myocardial insult and creatinine and blood urea nitrogen can ascertain the extent of renal dysfunction. Physiologically stressed infants rapidly deplete glucose stores and can develop profound hypoglycemia. Frequent blood glucose checks during the critical period of resuscitation are recommended.[7][8][9][8]

Treatment / Management

Therapeutic hypothermia is the treatment for neonatal hypoxic-ischemic encephalopathy. Following the immediate primary neuronal injury, during which there is an interruption of oxygen and glucose to the brain, there is a latent period of up to 6 hours before a secondary phase of injury occurs as the injured areas are reperfused, and damaged cells lyse, releasing toxic neurotransmitters. The goal of therapeutic hypothermia is to intervene during the latent period and minimize damage from the secondary neuronal injury. Therapeutic hypothermia, when started within six hours of injury decreases mortality and severe disability from 62% to 48% and increases survival with the normal outcome from 24% to 40% with a number needed to treat of six to seven. Whole body cooling appears to be more effective at decreasing death than selective head cooling, but both modalities are effective at decreasing severe disability and a combined outcome of death and severe disability. Infants with moderate encephalopathy (Sarnat Stage II) benefit most from therapeutic hypothermia. Importantly, cooling does not appear to decrease death at the cost of more severely neurologic impairment in survivors. Side effects associated with therapeutic hypothermia include peripheral vasoconstriction, diuresis, cardiac dysfunction, arrhythmias, coagulopathy, thrombocytopenia, stridor, leukocyte dysfunction, pulmonary hypertension and subcutaneous fat necrosis (calcium deposits in the skin). Therapeutic hypothermia can be delivered safely with specialized equipment and monitoring in sophisticated medical centers. [10][11][12][13][14]

The treatment of respiratory distress, pulmonary hypertension, coagulopathy and myocardial dysfunction is supportive. Infants with respiratory distress and pulmonary hypertension may require intubation, surfactant, oxygen and inhaled nitric oxide. Coagulopathy is treated with the prudent use of blood products to maintain oxygen-carrying capacity and coagulation. Myocardial dysfunction may result in a need for vasopressors. Renal dysfunction may result in oliguria or anuria; therefore, use of crystalloid fluid and blood products should be cautious.

Differential Diagnosis

  • Brain tumors
  • Developmental defects
  • Genetics of Methylmalonic acidemia
  • Genetics of Propionic acidemia
  • Infections
  • Neuromuscular disorders including neonatal myopathy

Enhancing Healthcare Team Outcomes

Birth asphyxia is not an uncommon event, and because of its high morbidity and mortality, the condition is best managed by an interprofessional team. However, the long-term prognosis of these infants has been difficult to assess. In the short term, the condition is reported to have a mortality in excess of 30%, with the majority of deaths occurring within the first few days after birth. Those infants who survive are often left with mild to severe neurological deficits, and they also end up dying from aspiration or systemic infections. Long-term survivors have been found to have disabling cerebral palsy, inadequate mental development or low psychomotor scores, seizures, blindness, and severe hearing impairment. The management of these infants, in the long run, is complex and prohibitively expensive. [3][15](Level V)

Review Questions

References

1.
Sugiura-Ogasawara M, Ebara T, Yamada Y, Shoji N, Matsuki T, Kano H, Kurihara T, Omori T, Tomizawa M, Miyata M, Kamijima M, Saitoh S., Japan Environment, Children’s Study (JECS) Group. Adverse pregnancy and perinatal outcome in patients with recurrent pregnancy loss: Multiple imputation analyses with propensity score adjustment applied to a large-scale birth cohort of the Japan Environment and Children's Study. Am J Reprod Immunol. 2019 Jan;81(1):e13072. [PMC free article: PMC6646903] [PubMed: 30430678]
2.
Hakobyan M, Dijkman KP, Laroche S, Naulaers G, Rijken M, Steiner K, van Straaten HLM, Swarte RMC, Ter Horst HJ, Zecic A, Zonnenberg IA, Groenendaal F. Outcome of Infants with Therapeutic Hypothermia after Perinatal Asphyxia and Early-Onset Sepsis. Neonatology. 2019;115(2):127-133. [PubMed: 30419568]
3.
Viaroli F, Cheung PY, O'Reilly M, Polglase GR, Pichler G, Schmölzer GM. Reducing Brain Injury of Preterm Infants in the Delivery Room. Front Pediatr. 2018;6:290. [PMC free article: PMC6198082] [PubMed: 30386757]
4.
Enweronu-Laryea CC, Andoh HD, Frimpong-Barfi A, Asenso-Boadi FM. Parental costs for in-patient neonatal services for perinatal asphyxia and low birth weight in Ghana. PLoS One. 2018;13(10):e0204410. [PMC free article: PMC6185862] [PubMed: 30312312]
5.
Kapaya H, Williams R, Elton G, Anumba D. Can Obstetric Risk Factors Predict Fetal Acidaemia at Birth? A Retrospective Case-Control Study. J Pregnancy. 2018;2018:2195965. [PMC free article: PMC6139200] [PubMed: 30245882]
6.
Odd D, Heep A, Luyt K, Draycott T. Hypoxic-ischemic brain injury: Planned delivery before intrapartum events. J Neonatal Perinatal Med. 2017;10(4):347-353. [PubMed: 29286930]
7.
Imai K, de Vries LS, Alderliesten T, Wagenaar N, van der Aa NE, Lequin MH, Benders MJNL, van Haastert IC, Groenendaal F. MRI Changes in the Thalamus and Basal Ganglia of Full-Term Neonates with Perinatal Asphyxia. Neonatology. 2018;114(3):253-260. [PMC free article: PMC6191878] [PubMed: 29961068]
8.
Salas J, Tekes A, Hwang M, Northington FJ, Huisman TAGM. Head Ultrasound in Neonatal Hypoxic-Ischemic Injury and Its Mimickers for Clinicians: A Review of the Patterns of Injury and the Evolution of Findings Over Time. Neonatology. 2018;114(3):185-197. [PubMed: 29936499]
9.
Alsaleem M, Zeinali LI, Mathew B, Kumar VHS. Glucose Levels during the First 24 Hours following Perinatal Hypoxia. Am J Perinatol. 2021 Apr;38(5):490-496. [PubMed: 31683321]
10.
Alsaleem M, Hpa N, Kumar VHS. Stridor in infants with hypoxic-ischemic encephalopathy and whole body hypothermia: A case series. J Neonatal Perinatal Med. 2020;13(4):463-468. [PubMed: 31985477]
11.
Kebaya LMN, Kiruja J, Maina M, Kimani S, Kerubo C, McArthur A, Munn Z, Ayieko P. Basic newborn resuscitation guidelines for healthcare providers in Maragua District Hospital: a best practice implementation project. JBI Database System Rev Implement Rep. 2018 Jul;16(7):1564-1581. [PMC free article: PMC7116459] [PubMed: 29995715]
12.
Simon LV, Hashmi MF, Bragg BN. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): May 27, 2021. APGAR Score. [PubMed: 29262097]
13.
Oliveira V, Singhvi DP, Montaldo P, Lally PJ, Mendoza J, Manerkar S, Shankaran S, Thayyil S. Therapeutic hypothermia in mild neonatal encephalopathy: a national survey of practice in the UK. Arch Dis Child Fetal Neonatal Ed. 2018 Jul;103(4):F388-F390. [PubMed: 28942433]
14.
Alsaleem M, Saadeh L, Elberson V, Kumar VHS. Subcutaneous fat necrosis, a rare but serious side effect of hypoxic-ischemic encephalopathy and whole-body hypothermia. J Perinat Med. 2019 Nov 26;47(9):986-990. [PubMed: 31586967]
15.
Riley C, Spies LA, Prater L, Garner SL. Improving Neonatal Outcomes Through Global Professional Development. Adv Neonatal Care. 2019 Feb;19(1):56-64. [PubMed: 30148727]
Copyright © 2021, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits use, duplication, adaptation, distribution, and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, a link is provided to the Creative Commons license, and any changes made are indicated.

Bookshelf ID: NBK430782PMID: 28613533

Views

  • PubReader
  • Print View
  • Cite this Page

Related information

  • PMC
    PubMed Central citations
  • PubMed
    Links to PubMed

Similar articles in PubMed

See reviews...See all...

Recent Activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...