Birth Asphyxia


Article Author:
Maria Gillam-Krakauer


Article Editor:
Clarence Gowen Jr


Editors In Chief:
Chaddie Doerr


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Frank Smeeks
Kristina Soman-Faulkner
Radia Jamil
Patrick Le
Sobhan Daneshfar
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Nazia Sadiq
Hajira Basit
Phillip Hynes
Tehmina Warsi


Updated:
12/2/2018 12:02:57 PM

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]

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, leukocyte dysfunction, pulmonary hypertension and sclerema (calcium deposits in the skin). Therapeutic hypothermia can be delivered safely with specialized equipment and monitoring in sophisticated medical centers. [9][10][11]

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.

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 a multidisciplinary 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][12](Level V)

 

 

 


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Birth Asphyxia - Questions

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Neonatal asphyxia is commonly associated with which of the following types of cerebral palsies?



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An infant admitted 3 hours earlier to the neonatal intensive care unit is exhibiting abnormal leg movements and chewing movements of the mouth. Apgars were 3 and 7. Pregnancy was normal, labor was prolonged and extraction difficult. Bedside glucose is normal. Which of the following tests should be ordered next?



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A 35-year-old G3P2002 presents at 39 weeks with severe abdominal pain and vaginal bleeding. Fetal heart rate is 100. A stat C-section is performed. The neonatal team is handed a pale, limp term infant with a heart rate of 40 and no spontaneous respiratory effort. The infant is aggressively resuscitated, including positive-pressure ventilation, intubation, umbilical venous line placement, epinephrine, normal saline bolus, and emergency release blood. The obstetrician confirms that a uterine rupture was the etiology of the vaginal bleeding prior to delivery. The first arterial blood gas was pH 6.9, pCO2 35, pO2 130, the base deficit -20 and lactate of 16. At one hour of age, she is breathing spontaneously and has a normal heart rate. She is lethargic but responsive and has overactive deep tendon reflexes, What is the most appropriate next course of action?



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Of the following, which is the most common cause of seizures in the early neonatal period?



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A male infant is born at 40 weeks by emergency cesarean delivery due to placental abruption. He receives positive pressure ventilation, chest compressions, and is endotracheally intubated. Apgar scores are 1, 1, and four at 1, 5, and 10 minutes, respectively. Upon examination at 30 minutes of age, he is breathing spontaneously but is lethargic with strong distal flexion, overactive reflexes, and miosis. Arterial blood gas is pH 6.9, pCO2 40, pO2 70, base deficit 20. Therapeutic hypothermia is started. What are the benefits of therapeutic hypothermia in this patient?



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Birth Asphyxia - References

References

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, 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. American journal of reproductive immunology (New York, N.Y. : 1989). 2018 Nov 14     [PubMed]
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. 2018 Nov 12     [PubMed]
Viaroli F,Cheung PY,O'Reilly M,Polglase GR,Pichler G,Schmölzer GM, Reducing Brain Injury of Preterm Infants in the Delivery Room. Frontiers in pediatrics. 2018     [PubMed]
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     [PubMed]
Kapaya H,Williams R,Elton G,Anumba D, Can Obstetric Risk Factors Predict Fetal Acidaemia at Birth? A Retrospective Case-Control Study. Journal of pregnancy. 2018     [PubMed]
Odd D,Heep A,Luyt K,Draycott T, Hypoxic-ischemic brain injury: Planned delivery before intrapartum events. Journal of neonatal-perinatal medicine. 2017     [PubMed]
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     [PubMed]
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     [PubMed]
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 of systematic reviews and implementation reports. 2018 Jul     [PubMed]
Simon LV,Bragg BN, APGAR Score null. 2018 Jan     [PubMed]
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. Archives of disease in childhood. Fetal and neonatal edition. 2018 Jul     [PubMed]
Riley C,Spies LA,Prater L,Garner SL, Improving Neonatal Outcomes Through Global Professional Development. Advances in neonatal care : official journal of the National Association of Neonatal Nurses. 2018 Aug 24     [PubMed]

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