Hubbry Logo
Perinatal asphyxiaPerinatal asphyxiaMain
Open search
Perinatal asphyxia
Community hub
Perinatal asphyxia
logo
7 pages, 0 posts
0 subscribers
Be the first to start a discussion here.
Be the first to start a discussion here.
Perinatal asphyxia
Perinatal asphyxia
Perinatal asphyxia
View on Wikipedia
from Wikipedia
Perinatal asphyxia
Other namesNeonatal asphyxia
SpecialtyPediatrics, obstetrics Edit this on Wikidata

Perinatal asphyxia (also known as neonatal asphyxia or birth asphyxia) is the medical condition resulting from deprivation of oxygen to a newborn infant that lasts long enough during the birth process to cause physical harm, usually to the brain. It remains a serious condition which causes significant mortality and morbidity. It is also the inability to establish and sustain adequate or spontaneous respiration upon delivery of the newborn, an emergency condition that requires adequate and quick resuscitation measures. Perinatal asphyxia is also an oxygen deficit from the 28th week of gestation to the first seven days following delivery. It is also an insult to the fetus or newborn due to lack of oxygen or lack of perfusion to various organs and may be associated with a lack of ventilation. In accordance with WHO, perinatal asphyxia is characterised by: profound metabolic acidosis, with a pH less than 7.20 on umbilical cord arterial blood sample, persistence of an Apgar score of 3 at the 5th minute, clinical neurologic sequelae in the immediate neonatal period, or evidence of multiorgan system dysfunction in the immediate neonatal period. Hypoxic damage can occur to most of the infant's organs (heart, lungs, liver, gut, kidneys), but brain damage is of most concern and perhaps the least likely to quickly or completely heal. In more pronounced cases, an infant will survive, but with damage to the brain manifested as either mental, such as developmental delay or intellectual disability, or physical, such as spasticity.

It results most commonly from antepartum causes like a drop in maternal blood pressure or some other substantial interference with blood flow to the infant's brain during delivery. This can occur due to inadequate circulation or perfusion, impaired respiratory effort, or inadequate ventilation. Perinatal asphyxia happens in 2 to 10 per 1000 newborns that are born at term, and more for those that are born prematurely.[1] WHO estimates that 4 million neonatal deaths occur yearly due to birth asphyxia, representing 38% of deaths of children under 5 years of age.[2]

Perinatal asphyxia can be the cause of hypoxic ischemic encephalopathy or intraventricular hemorrhage, especially in preterm births. An infant with severe perinatal asphyxia usually has poor color (cyanosis), perfusion, responsiveness, muscle tone, and respiratory effort, as reflected in a low 5 minute Apgar score. Extreme degrees of asphyxia can cause cardiac arrest and death. If resuscitation is successful, the infant is usually transferred to a neonatal intensive care unit.

There has long been a scientific debate over whether newborn infants with asphyxia should be resuscitated with 100% oxygen or normal air.[3] It has been demonstrated that high concentrations of oxygen lead to generation of oxygen free radicals, which have a role in reperfusion injury after asphyxia.[4] Research by Ola Didrik Saugstad and others led to new international guidelines on newborn resuscitation in 2010, recommending the use of normal air instead of 100% oxygen.[5][6]

There is considerable controversy over the diagnosis of birth asphyxia due to medicolegal reasons.[7][8] Because of its lack of precision, the term is eschewed in modern obstetrics.[9]

Cause

[edit]

Basically, understanding of the etiology of perinatal asphyxia provides the platform on which to build on its pathophysiology. The general principles guiding the causes and the pathophysiology of perinatal asphyxia are grouped into antepartum causes and intra partum causes. As these are the various points to which insults can occur to the foetus. [citation needed]

  • Antepartum causes
  • Intra partum causes
    • Inadequate relaxation of uterus due to excess oxytocin
    • Prolonged delivery
    • Knotting of umbilical cord around the neck of infant

Risk factors

[edit]
  • Elderly or young mothers
  • Prolonged rupture of membranes
  • Meconium-stained fluid
  • Multiple births
  • Lack of antenatal care
  • Low birth weight infants
  • Malpresentation
  • Augmentation of labour with oxytocin
  • Antepartum hemorrhage
  • Severe eclampsia and pre-eclampsia
  • Antepartum and intrapartum anemia[10]

Treatment

[edit]
  • A= Establish open airway: Suctioning, if necessary endotracheal intubation
  • B= Breathing: Through tactile stimulation, PPV, bag and mask, or through endotracheal tube
  • C= Circulation: Through chest compressions and medications if needed
  • D= Drugs: Adrenaline .01 of .1 solution
  • Hypothermia treatment to reduce the extent of brain injury
  • Epinephrine 1:10000 (0.1-0.3ml/kg) IV
  • Saline solution for hypovolemia

Epidemiology

[edit]
Disability-adjusted life year for birth asphyxia and birth trauma per 100,000 inhabitants in 2002

A 2008 bulletin from the World Health Organization estimates that 900,000 total infants die each year from birth asphyxia, making it a leading cause of death for newborns.[11]

In the United States, intrauterine hypoxia and birth asphyxia was listed as the tenth leading cause of neonatal death.[12]

Medicolegal aspects

[edit]

There is current controversy regarding the medicolegal definitions and impacts of birth asphyxia. Plaintiff's attorneys often take the position that birth asphyxia is often preventable, and is often due to substandard care and human error.[13] They have utilized some studies in their favor that have demonstrated that, "... although other potential causes exist, asphyxia and hypoxic-ihy affect a substantial number of babies, and they are preventable causes of cerebral palsy."[14][15][16] The American Congress of Obstetricians and Gynecologists disputes that conditions such as cerebral palsy are usually attributable to preventable causes, instead associating them with circumstances arising prior to birth and delivery.[17]

References

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Perinatal asphyxia

View on Grokipedia
from Grokipedia
Perinatal asphyxia, also known as birth asphyxia or neonatal asphyxia, is a medical condition characterized by the deprivation of oxygen and blood flow to a newborn before, during, or immediately after birth, leading to (low blood oxygen levels) and (buildup of acid in the blood). This oxygen deprivation can result in hypoxic-ischemic (HIE), a type of , and affects multiple organ systems if not addressed promptly.

Historical Background

The condition has been recognized since antiquity, but the term "birth asphyxia" emerged in the , replacing "apparent death of the newborn" amid fears of . Modern understanding advanced with 20th-century developments in fetal monitoring and , and the formalized aspects of the definition in 1997 to encompass failure to establish breathing at birth. Globally, perinatal asphyxia accounts for approximately 900,000 neonatal deaths annually (as of recent WHO estimates), representing a leading cause of early neonatal mortality, particularly in low-resource settings where incidence rates can reach 20 per 1,000 live births compared to 2 per 1,000 in high-resource countries. It primarily arises from complications interrupting fetal oxygen supply, such as placental issues or labor dystocia, with antepartum factors contributing in about 20% of cases and intrapartum events in the majority. Prompt and interventions like therapeutic can mitigate brain damage, though survivors may face long-term neurologic deficits, with 15-20% mortality in the neonatal period. Prevention focuses on antenatal care, skilled delivery, and access to emergency services.

Introduction

Definition

Perinatal asphyxia refers to the deprivation of oxygen (hypoxia or anoxia) and/or reduced blood flow (ischemia) to the or newborn in the immediate period surrounding birth, which can result in systemic and neurological injury. This condition arises from an interruption in or fetal oxygenation during the perinatal phase, potentially leading to and if severe. Common synonyms for perinatal asphyxia include birth asphyxia and neonatal , while the term hypoxic-ischemic encephalopathy (HIE) is specifically used when there is prominent neurological involvement due to from the hypoxic-ischemic event. The scope of perinatal asphyxia encompasses the antepartum (before labor), intrapartum (during labor and delivery), and postpartum (immediately after birth) periods, focusing on acute events rather than chronic fetal hypoxia, such as that seen in prolonged . Diagnosis of perinatal asphyxia is often associated with low Apgar scores, such as a score of less than 5 at 5 minutes of age, indicating poor adaptation to extrauterine life, though Apgar scores alone are not sufficient for definitive diagnosis and must be considered alongside other clinical evidence. This criterion helps identify newborns at risk but underscores the need for a multifaceted assessment to confirm the presence and severity of .

Historical Background

The concept of perinatal asphyxia originated in the as " of the newborn," a term arising amid widespread European fears of , which prompted early efforts in to distinguish stillborn infants from those merely appearing lifeless. This diagnosis was initially linked to impaired placental respiration, even before the discovery of oxygen in the late , and reflected a growing medical interest in distinguishing recoverable newborns from the truly deceased. By the late 1700s, the term evolved into "birth asphyxia," recognizing oxygen deprivation as the underlying cause, with classifications like "blue" (cyanotic) and "white" (pale) asphyxia emerging to describe clinical presentations. In the 19th and early 20th centuries, understanding advanced with the identification of oxygen deprivation's role in neonatal distress, shifting focus from or accidental causes to physiological ones, though blame often fell on midwives and obstetricians for perceived mishandling of deliveries. A pivotal development came in 1953 when anesthesiologist introduced the , a standardized 10-point assessment of newborn vitality at one and five minutes post-birth, evaluating appearance, , grimace, activity, and respiration to guide immediate interventions and quantify severity. This tool marked a transition toward objective evaluation, reducing subjective blame and enabling better practices. By the late 20th century, the terminology and perspective shifted further from broad "birth asphyxia" to evidence-based recognition of hypoxic-ischemic encephalopathy (HIE) as a specific brain injury pattern resulting from perinatal oxygen and blood flow deprivation, diminishing earlier tendencies to attribute outcomes solely to practitioner error. In the post-2000 era, this understanding spurred the adoption of neuroprotective therapies, notably therapeutic hypothermia, following landmark randomized trials in the mid-2000s that demonstrated its efficacy in reducing mortality and neurodevelopmental disability in moderate to severe HIE cases when initiated within six hours of birth. The World Health Organization highlighted perinatal asphyxia as a major global neonatal killer in early 2000s reports, estimating around 900,000 annual deaths and underscoring the need for improved prevention and intervention strategies.

Etiology

Causes

Perinatal asphyxia arises from events that disrupt oxygen delivery to the or newborn, primarily through impaired blood flow or across the or in the immediate postnatal period. These causes are categorized by timing relative to delivery: antepartum (before labor), intrapartum (during labor), and postpartum (after birth). Intrapartum events account for the majority of cases (estimates vary, with antepartum causes representing about 20% in some sources), while postpartum issues are less common (around 10%) but critical in the early neonatal period. Intrapartum causes, occurring during labor and delivery, are the most frequent precipitants of oxygen deprivation and often coincide with the second stage of labor when fetal expulsion occurs. Key examples include , which leads to acute hemorrhage and reduced uteroplacental perfusion; , causing separation of the placenta from the uterine wall and interrupting blood flow; or compression, which obstructs venous return and arterial supply to the ; and , where delayed delivery compresses the cord against the maternal . These sentinel events can result in near-total if not rapidly addressed. Antepartum causes involve chronic or acute insults prior to the onset of labor, leading to progressive fetal hypoxia. Maternal , such as from or , reduces placental perfusion and oxygen transfer. , often due to vascular abnormalities or , impairs nutrient and oxygen exchange across the . Fetal-maternal hemorrhage, where fetal blood enters the maternal circulation, causes acute fetal and , severely limiting oxygen-carrying capacity. Postpartum causes emerge immediately after birth and can exacerbate or independently cause through respiratory or circulatory failure. Airway obstruction, such as from congenital malformations or retained amniotic debris, prevents effective ventilation. Severe , often from unresolved antepartum hemorrhage or birth trauma, diminishes the newborn's ability to transport oxygen to tissues. Additionally, meconium aspiration, where the newborn inhales meconium-stained during or just after delivery, leads to airway blockage, , and respiratory compromise, particularly in stressed fetuses during .

Risk Factors

Risk factors for perinatal asphyxia encompass a range of maternal, fetal, obstetric, and preconceptional conditions that increase the likelihood of oxygen deprivation to the during the perinatal period. These predispositions highlight the importance of antenatal screening and monitoring to mitigate potential complications. Maternal factors include greater than 35 years, which is associated with higher rates of and fetal distress leading to . in the mother reduces oxygen-carrying capacity to the , elevating risk. Hypertensive disorders such as impair uteroplacental blood flow, contributing to hypoxia. Maternal infections, including chorioamnionitis, trigger inflammatory responses that compromise fetal oxygenation. Substance use, particularly , induces and abruptio placentae, further predisposing to asphyxial events. Fetal factors involve (IUGR), where limits nutrient and oxygen supply, heightening vulnerability to during labor. Post-term pregnancy beyond 42 weeks increases risks due to placental aging and reduced efficiency. Multiple gestations, such as twins, are linked to higher incidence owing to shared placental resources and preterm delivery complications. Congenital anomalies, including cardiac defects, can exacerbate intrapartum stress and oxygen demand mismatches. Obstetric factors encompass exceeding 24 hours, which exhausts fetal reserves and promotes . Abnormal presentations like breech position complicate delivery and elevate cord compression risks. Meconium-stained signals fetal distress and is correlated with higher rates, often necessitating urgent intervention. Preconceptional elements such as low and inadequate amplify overall vulnerability, with higher prevalence in low-resource settings due to delayed access to monitoring and interventions.

Pathophysiology

Mechanisms

Perinatal asphyxia initiates a hypoxic-ischemic characterized by reduced oxygen delivery to tissues, prompting a shift to anaerobic metabolism, accumulation of , and depletion of (ATP). This energy failure disrupts cellular , as halts in mitochondria, leading to impaired pumps and collapse. In the , this particularly targets vulnerable regions such as the hippocampus and , where high metabolic demands exacerbate the effects. The primary phase of injury involves immediate neuronal due to profound energy failure, manifesting as in severely affected areas or in less intense zones. Necrotic cells swell and rupture, releasing contents that amplify damage, while apoptotic pathways activate through cascades in structures like the hippocampal . This phase occurs during the acute hypoxic event, with selective vulnerability in neurons reliant on aerobic . Upon reoxygenation, exacerbates damage through (ROS) production from mitochondrial electron transport chains, causing , protein oxidation, and DNA fragmentation. arises from excessive glutamate release, overstimulating NMDA receptors and triggering calcium influx that propagates . Concurrently, intensifies with microglial activation, infiltration, and release shortly after the insult. Beyond the , the hypoxic-ischemic cascade induces multi-organ dysfunction, including cardiac from reperfusion-mediated myocardial that reduces output. Renal tubular necrosis results from ischemic hypoperfusion, leading to in up to 44% of cases. Hepatic involvement manifests as elevation due to hypoperfusion-induced hepatocyte damage, affecting 57% of neonates with .

Stages and Injury Patterns

Perinatal asphyxia progresses through distinct temporal phases of brain injury, primarily characterized by energy failure and cellular damage in the context of hypoxic-ischemic encephalopathy (HIE). The primary phase occurs within minutes of the acute hypoxic-ischemic insult, involving immediate deprivation of oxygen and glucose, leading to anaerobic metabolism, ATP depletion, and failure of the Na+/K+ ATPase pump. This results in neuronal , cytotoxic , and initial cell death through and early . Following the primary phase, a latent phase ensues, typically lasting 1 to 6 hours after partial restoration of cerebral flow, during which there is an apparent clinical recovery with normalization of cerebral energy metabolism. However, subclinical processes such as ongoing and initiation of apoptotic cascades continue, representing a potential therapeutic window before further deterioration. The secondary phase develops 6 to 48 hours post-insult, peaking between 24 and 72 hours, and is marked by delayed secondary failure driven by , including , excitotoxicity from excessive glutamate release, and inflammatory responses. These mechanisms culminate in , further , and , exacerbating neuronal loss independent of the initial . A tertiary phase extends from days to months or even years after the insult, involving persistent , impaired and oligodendrogenesis, blood-brain barrier disruption, and epigenetic modifications that contribute to long-term neurodegeneration and neurodevelopmental impairments. Injury patterns in perinatal asphyxia vary by and insult severity, reflecting selective vulnerability of brain regions. In term infants (≥36 weeks), partial prolonged hypoxia commonly produces watershed injuries affecting the parasagittal cortex and subcortical , visible on MRI as diffusion restriction and later or ulegyria in vulnerable border zones between major arterial territories. In contrast, preterm infants exhibit predominant periventricular injury, such as , due to the immaturity of and vascular supply in this region, leading to cystic changes and on imaging. The severity of HIE resulting from perinatal asphyxia is often classified using the system, which integrates clinical and electroencephalographic features across three stages. Stage I (mild) involves hyperalertness, normal EEG, and lasting less than 24 hours, with full recovery expected. Stage II (moderate) features , , seizures, and periodic EEG patterns, typically resolving within days but associated with potential neurodevelopmental risks. Stage III (severe) presents with stupor, flaccidity, suppressed reflexes, and suppressed or isoelectric EEG, correlating with high mortality or profound impairment.

Diagnosis

Clinical Signs

Perinatal asphyxia in newborns is characterized by immediate clinical signs reflecting acute oxygen deprivation and metabolic derangement at birth. These include low Apgar scores at 5 minutes (0-3 for more than 5 minutes), indicating poor , respiratory effort, , irritability, and color. Affected infants often present with a weak or absent cry, (floppy appearance), ( below 100 beats per minute), and central due to inadequate oxygenation. These signs arise from the pathophysiological interruption of fetal oxygenation, leading to rapid decompensation in the immediate postnatal period. Neurological manifestations are prominent and may evolve over the first hours to days. Common findings include altered levels of , ranging from to , and seizures, which can be overt (clonic or tonic) or subtle (e.g., lip smacking or pedaling movements). In the recovery phase, some infants develop or exaggerated reflexes as subsides. These neurological signs reflect hypoxic-ischemic injury to the , often culminating in if severe. Systemic signs indicate multi-organ involvement beyond the . Respiratory distress is frequent, featuring grunting respirations, apnea, or irregular gasping due to pulmonary immaturity or aspiration. with arterial below 7.0 is a hallmark, often accompanied by signs of renal dysfunction such as (urine output less than 1 mL/kg/hour). Other systemic features may include hepatic elevation or myocardial dysfunction, manifesting as poor or . The severity of encephalopathy is commonly graded using the Sarnat clinical staging system, which categorizes findings into three levels based on within the first 24 hours.
StageLevel of ConsciousnessMuscle TonePostureStretch ReflexesComplex ReflexesSeizures
I (Mild)Hyperalert to irritableNormalNormalNormal or increasedWeak suck; strong Moro; mild tonic neckNone
II (Moderate)Lethargic or obtundedDistal flexion (decorticate)Decreased or increasedWeak or absent suck and Moro; strong tonic neckFrequent, focal or multifocal
III (Severe)FlaccidDecerebrateHypoactive or absentAbsent suck, Moro, and tonic neckUncommon or delayed
This staging aids in prognostic assessment, with Stage I often resolving without sequelae, while Stages II and III correlate with higher risks of neurological impairment.

Diagnostic Tests

Diagnosis of perinatal asphyxia involves , , and monitoring tools to objectively confirm the presence and severity of hypoxic-ischemic injury following clinical suspicion. These tests provide quantitative evidence of , , and neurological damage, aiding in differentiation from other neonatal conditions. Blood gas analysis is a cornerstone for immediate assessment, particularly through umbilical cord arterial samples obtained at birth. A below 7.0 combined with a of -12 mmol/L or lower indicates severe reflective of perinatal asphyxia. Elevated lactate levels exceeding 4 mmol/L in further corroborate hypoxic stress, with higher values correlating to increased risk of neonatal complications. Postnatal gas monitoring continues to track acid-base status and guide supportive care, distinguishing metabolic from . Biomarkers offer insights into specific organ injury, particularly the brain and heart. Neuron-specific enolase (NSE), a marker of neuronal damage, rises in serum within 4-72 hours post-asphyxia; levels above 40 mcg/L help differentiate moderate to severe hypoxic-ischemic encephalopathy (HIE) from milder cases. Similarly, S100B protein, released from astroglial cells, is elevated in cord or serum blood during the first 72 hours, with concentrations over 2.02 μg/L in cord blood showing high sensitivity (86.7%) and specificity (88%) for moderate to severe HIE. For cardiac involvement, troponin levels are measured to detect myocardial ischemia, often rising due to hypoxic stress on the heart. Imaging modalities provide structural and functional evaluation of brain injury. (MRI), ideally performed 5-10 days after the insult, is the preferred tool for visualizing characteristic patterns such as and thalamic lesions in term infants with HIE; diffusion-weighted imaging can detect acute changes as early as 24-48 hours. (EEG), including amplitude-integrated EEG (aEEG), is used for real-time monitoring of cerebral activity, identifying seizures and abnormal patterns like that indicate severity, with aEEG sensitivity up to 91% for poor outcomes. Additional tests include the lactate/pyruvate ratio from , where a ratio greater than 22 signals anaerobic from hypoxia, enhancing diagnostic accuracy when combined with and . To exclude differentials such as , blood cultures and inflammatory markers like are employed alongside the above, as clinical overlap may occur but specific patterns and imaging favor .

Management

Initial Resuscitation

Initial resuscitation in the delivery room is a time-sensitive intervention for newborns with perinatal asphyxia, focusing on rapid restoration of vital functions to prevent further hypoxic-ischemic injury. The (NRP), endorsed by the (AHA), provides evidence-based guidelines that emphasize a systematic starting immediately after birth. The first steps involve warming the newborn to prevent , thoroughly drying the skin to stimulate breathing and remove , and providing tactile stimulation such as rubbing the back or soles of the feet; these actions must begin within of delivery. According to (WHO) guidelines, these basic measures suffice for approximately 90% of newborns needing assistance at birth, particularly in resource-limited settings where advanced equipment may be unavailable. If the newborn's is below 100 beats per minute after initial assessment and stimulation, positive pressure ventilation (PPV) is initiated promptly using a self-inflating bag or T-piece resuscitator with room air (21% oxygen) for term infants, with titration of blended oxygen as needed based on response, while monitoring preductal to target 85-95% by 10 minutes of life to avoid . Effective PPV requires proper airway positioning (neutral head position with slight extension), clearance of secretions if present, and an initial inflation pressure of 20-25 cm H2O for term infants; endotracheal is indicated if mask ventilation fails to improve or oxygenation after 30 seconds. (ECG) is recommended to confirm before initiating chest compressions. For persistent with less than 60 beats per minute despite 60 seconds of effective PPV, chest compressions are commenced using the two-thumb encircling technique around the lower third of the , coordinated with ventilations at a 3:1 ratio to achieve 90 compressions and 30 breaths per minute. If the remains below 60 beats per minute after 60 seconds of coordinated compressions and ventilation, intravenous epinephrine is administered at a dose of 0.01-0.03 mg/kg via the umbilical venous , with repeat doses every 3-5 minutes if needed. In cases of suspected , such as or poor response to initial measures, volume expansion with 10 mL/kg of isotonic crystalloid (e.g., normal saline) is given intravenously over 5-10 minutes, followed by reassessment. Throughout the process, a multidisciplinary approach is essential, with continuous monitoring of , respiratory effort, and color to guide progression through these steps.

Therapeutic Hypothermia

Therapeutic hypothermia is an evidence-based neuroprotective intervention for term neonates with moderate-to-severe hypoxic-ischemic (HIE) resulting from perinatal asphyxia, aimed at reducing injury by slowing metabolic processes and limiting secondary damage following the initial hypoxic insult. The protocol involves controlled whole-body cooling to a target core temperature of 33–34°C for 72 hours, initiated as soon as possible but within 6 hours of birth to maximize efficacy. Eligibility is restricted to infants at ≥35 weeks and >1800 g who meet criteria for moderate-to-severe HIE, typically confirmed by clinical encephalopathy scoring (e.g., modified Sarnat stage 2 or 3) and evidence of intrapartum asphyxia such as umbilical cord arterial pH <7.0 or base deficit ≥12 mmol/L. Cooling is achieved using servo-controlled devices, such as cooling blankets with pads and rectal temperature probes for precise regulation, or non-invasive methods like ice packs wrapped in for initial stabilization if specialized is unavailable. Following the 72-hour cooling period, rewarming occurs gradually at a rate of 0.5°C per hour over 6–12 hours to prevent rebound or seizures, with continuous monitoring of , cardiac rhythm, coagulation parameters, and electrolytes to manage common side effects such as , thrombocytopenia, and mild . Major randomized controlled trials, including the TOBY (Total Body Hypothermia for Neonatal Encephalopathy) and NICHD (National Institute of Child Health and Human Development) studies, along with meta-analyses, demonstrate that reduces the combined risk of death or major neurodevelopmental disability by approximately 25–32% at 18–24 months in eligible infants. For moderate HIE, the is around 33%, compared to 17% for severe cases, with the being 6–7 to prevent one adverse outcome. Contraindications include mild HIE (Sarnat stage 1), <35 weeks, <1800 g, and significant congenital anomalies or conditions precluding survival; preterm infants are excluded due to higher risks of adverse effects without proven benefit. Adjunct therapies, such as high-dose , remain under investigation in ongoing trials to potentially enhance , though recent phase III studies like HEAL have not yet shown definitive additive benefits.

Prognosis and Outcomes

Mortality and Morbidity

Perinatal asphyxia is associated with significant short-term mortality, with case fatality rates among affected neonates ranging from 15% to 20%. In cases progressing to severe hypoxic-ischemic encephalopathy (HIE), mortality exceeds 30%, often reaching 25-50%. The majority of these deaths occur within the first 72 hours of life, primarily due to multi-organ failure or overwhelming systemic complications. Globally, perinatal asphyxia accounts for an estimated 500,000 neonatal deaths annually (as of ), representing a substantial burden particularly in resource-limited settings. Acute morbidity in surviving neonates frequently involves multi-organ dysfunction, affecting up to 55% of cases and leading to immediate threats to vital systems. Renal involvement, such as , occurs in approximately 50% of asphyxiated infants, often manifesting as elevated creatinine levels and . Cardiac complications, including myocardial dysfunction and , are reported in about 30-55% of cases, contributing to hemodynamic instability. Seizures, a hallmark of moderate-to-severe HIE, arise in 50-70% of affected neonates, typically within the first days and requiring prompt intervention. Mortality and morbidity rates are heavily influenced by asphyxia severity and healthcare access. For instance, neonates classified under Sarnat III (severe HIE) face mortality rates approaching 70%, far higher than milder stages. In low-income settings, outcomes are worse due to delayed and limited intensive care, with contributing to over half of neonatal deaths in these regions. Recent trends indicate declining mortality in high-resource settings due to increased use of therapeutic , with rates dropping from around 17.5% in moderate/severe HIE cases in 2011 to lower levels by 2021; however, in low- and middle-income countries, outcomes remain poor, and recent trials (as of 2024) show limited benefit or potential harm from . These immediate risks underscore the need for rapid intervention, though long-term sequelae may also emerge in survivors.

Long-term Effects

Survivors of perinatal asphyxia often face significant neurological sequelae, including , which affects 10-20% of survivors of moderate to severe HIE, manifesting as persistent motor dysfunction due to brain injury sustained during the hypoxic-ischemic event. is another common long-term outcome, occurring in 10-30% of survivors, with higher rates associated with moderate to severe hypoxic-ischemic encephalopathy (HIE). Cognitive impairments are prevalent as well, with 15-25% of survivors exhibiting moderate to severe delays, often defined as an IQ below 70-85 on standardized assessments, impacting learning and adaptive functioning into and adulthood. Sensory and motor deficits further compound these challenges; visual impairments, such as cortical visual dysfunction, and occur in a notable proportion of survivors, estimated at 3-10% for hearing deficits alone, often requiring ongoing interventions like hearing aids or visual aids. In severe cases, particularly those involving profound asphyxia, spastic quadriplegia—a form of characterized by increased and impaired mobility in all four limbs—develops, leading to profound physical limitations and dependency on assistive devices. Predictors of these long-term effects include specific patterns observed on (MRI), where and thalamic injuries are strongly linked to motor deficits like and , while watershed injuries correlate more with cognitive impairments. Therapeutic hypothermia, when initiated promptly in moderate to severe HIE, improves neurodevelopmental outcomes by reducing the of death or major by approximately 25%, as evidenced by meta-analyses of randomized trials. Long-term follow-up is essential for early detection and management, utilizing tools such as the Bayley Scales of Infant and Toddler Development to assess neurodevelopmental progress; in moderate HIE, about 25% of survivors exhibit permanent deficits, necessitating multidisciplinary support including , educational accommodations, and .

Epidemiology

Incidence Rates

Perinatal asphyxia affects approximately 2 to 5 per 1,000 live births in high-resource countries, while incidence rates are substantially higher at 10 to 20 per 1,000 live births in low-resource settings, such as . The subset of cases leading to hypoxic-ischemic encephalopathy (HIE) occurs in 1 to 8 per 1,000 term births globally, with rates of about 1.5 per 1,000 live births in developed nations. Incidence of HIE has declined in developed countries due to advancements in obstetric care, with some regions reporting roughly a 50% reduction since the . Demographic factors influence occurrence, with higher rates observed among male infants and those with . The annual global burden is estimated at 1 to 2 million cases of due to birth and trauma. According to data from the 2020s, perinatal accounts for about 24% of neonatal deaths worldwide, contributing to nearly 900,000 annual fatalities. These rates exhibit regional variations, with the highest burdens in low- and middle-income countries.

Global Disparities

Perinatal asphyxia disproportionately affects low- and middle-income countries (LMICs), where over 90% of the global occurs, with incidence rates 5 to 20 times higher than in high-income countries (HICs). In LMICs, birth accounts for approximately 24% of all neonatal deaths, reflecting limited access to emergency obstetric care and facilities. For instance, in , perinatal asphyxia contributes to about 40% of neonatal mortality, exacerbating the region's high overall newborn death rates of 21 per 1,000 live births. These disparities underscore how resource constraints in LMICs lead to preventable intrapartum complications that are largely mitigated in wealthier settings. In HICs, the incidence of perinatal asphyxia is significantly lower, at 1 to 3 per 1,000 term births, primarily due to widespread availability of cesarean sections (with rates averaging 23% and procedures comprising 20-30% in many developed nations) and advanced fetal monitoring technologies that enable timely interventions. However, even within HICs, socioeconomic and racial disparities persist, with higher rates observed among minority populations; for example, Black and Indigenous infants experience elevated neonatal mortality risks, including from asphyxia-related causes, linked to systemic barriers in prenatal and intrapartum care. Key contributing factors to these global inequities include unequal access to skilled birth attendants, higher maternal infection rates in resource-poor areas, and , which impair fetal oxygenation and increase vulnerability to hypoxic events. The has further widened these gaps, with disruptions to healthcare services in LMICs leading to increased perinatal risks, including a reported rise in neonatal during lockdowns due to delayed presentations and reduced monitoring. Projections under the (SDG 3.2) aim to reduce overall neonatal mortality to 12 or fewer deaths per 1,000 live births by 2030 through targeted interventions like improved obstetric training and facility upgrades, which could substantially alleviate the burden in LMICs if scaled effectively.

Prevention

Antenatal Measures

Antenatal measures encompass a range of prenatal screening and care strategies aimed at identifying and mitigating risks that could lead to perinatal asphyxia, focusing on optimizing fetal well-being before labor onset. These interventions primarily target modifiable risk factors such as , conditions, and infections, thereby reducing the incidence of antepartum hypoxia. By promoting early detection and intervention, antenatal care helps prevent the progression of conditions like (IUGR) that may culminate in during delivery. Routine prenatal screening forms the cornerstone of these preventive efforts. Obstetric examinations are routinely performed to assess fetal growth and detect IUGR, which is associated with chronic and increased risk of ; serial s in the third trimester can identify Doppler abnormalities in flow, prompting timely management. Maternal screening through complete blood counts at initial and subsequent visits is essential, as untreated can impair oxygen delivery to the , exacerbating hypoxic risks—iron supplementation is recommended when levels fall below 11 g/dL. Additionally, infection prophylaxis includes universal screening for (GBS) between 36 0/7 and 37 6/7 weeks of gestation via vaginal-rectal swabs, with intrapartum antibiotic administration for positive cases to prevent that could contribute to asphyxial events. For high-risk pregnancies, intensified monitoring protocols are implemented to closely surveil fetal status. Serial non-stress tests (NSTs), typically starting at 32 weeks in cases of suspected IUGR or maternal conditions like , evaluate fetal reactivity to assess oxygenation and acid-base balance; non-reactive patterns may indicate the need for further evaluation or delivery planning. Biophysical profiles, combining NST with assessment of fetal movements, breathing, tone, and volume, provide a comprehensive score (out of 10) to gauge fetal compromise—scores of 6/10 are equivocal and require repeat testing or additional assessment, while scores of 4/10 or less indicate fetal compromise warranting prompt intervention. Folic acid supplementation, recommended at 400-800 mcg daily from preconception through the first trimester, reduces the risk of defects and associated congenital anomalies that could indirectly heighten vulnerability by complicating fetal development. Professional guidelines emphasize structured to maximize these preventive benefits. As of 2025, the American College of Obstetricians and Gynecologists (ACOG) advocates for tailored prenatal care delivery, with an initial comprehensive ideally before 10 weeks of , adjusting frequency and modality based on individual factors, , and ongoing needs; this personalized approach replaces fixed schedules for high-risk cases, incorporating more frequent assessments as required (e.g., biweekly from 28 weeks). The (WHO) similarly recommends a minimum of eight contacts, starting in the first trimester, to facilitate early screening and education on modifiable s. counseling is a key component, offered at every visit for tobacco-using pregnant individuals, as maternal increases the odds of and placental issues by up to 2-fold, thereby elevating —behavioral interventions combined with replacement can achieve quit rates of 10-20%. The collective impact of these antenatal measures is substantial, with evidence indicating that comprehensive antenatal care is associated with reduced risks of perinatal and neonatal mortality, primarily via improved management of IUGR and infections. These outcomes underscore the value of proactive prenatal strategies in averting potentially devastating fetal compromise.

Intrapartum Interventions

Intrapartum interventions aim to detect and mitigate fetal hypoxia during labor, thereby preventing or limiting the progression of perinatal asphyxia. Continuous (CTG) is recommended for high-risk pregnancies, where it monitors fetal patterns to identify potential distress early. In cases of abnormal CTG tracings, such as persistent decelerations, fetal scalp blood sampling for assessment can provide an adjunctive measure of fetal acid-base status, guiding decisions on the need for expedited delivery. A below 7.20 typically indicates and warrants intervention to avert worsening asphyxia. Obstetric maneuvers are essential when monitoring reveals fetal distress. Timely cesarean section is indicated for non-reassuring fetal status, including prolonged second of labor exceeding three hours in nulliparous women or two hours in multiparous women, as delays can exacerbate hypoxia. Proper cord , such as immediate recognition and elevation of the presenting part in suspected cord , helps maintain placental blood flow and reduces the risk of acute . These actions prioritize rapid intervention to restore oxygenation. Guidelines from the International Federation of Gynecology and Obstetrics (FIGO) and the (WHO) emphasize standardized intrapartum care, including the use of the WHO Labour Care Guide—a graphical tool that tracks labor progress, fetal wellbeing, and maternal status to facilitate timely decisions. FIGO's consensus on intrapartum fetal monitoring advocates for CTG in high-risk cases while cautioning against overuse in low-risk labors to avoid iatrogenic complications like unnecessary cesareans. Evidence from systematic reviews indicates that continuous CTG compared to intermittent reduces neonatal seizures by approximately 50%, though it does not significantly alter overall rates.

Medicolegal Aspects

One of the primary legal challenges in perinatal asphyxia litigation involves disputes over causation, particularly distinguishing intrapartum hypoxia from antepartum origins of the injury. Plaintiffs must demonstrate that the hypoxic event occurred during labor and delivery rather than earlier in , often relying on fetal monitoring and neonatal outcomes. However, courts frequently reject claims due to insufficient linking substandard care to the specific timing of the , with studies showing that lack of causal relation accounts for approximately 95% of denied compensation requests in asphyxia cases. Apgar scores are commonly contested in these disputes as non-specific indicators of , since low scores can result from various factors unrelated to intrapartum hypoxia, leading to misconceptions that fuel undeserved suits. Negligence claims in perinatal asphyxia cases often center on failures in fetal monitoring and timely interventions, such as delayed cesarean sections or misinterpretation of cardiotocography (CTG) traces. Inadequate CTG monitoring, including failure to respond to pathological fetal heart rate patterns or poor trace quality, has been identified as the primary factor in nearly 90% of compensated claims, contributing to delayed delivery in over 80% of instances. Civil courts recognize a causal link between such negligence and asphyxia in about 62% of cases where professional inadequacy is established, compared to 25% in penal proceedings, reflecting stricter evidentiary standards in criminal matters that vary by jurisdiction. In the United States, successful malpractice suits for these failures typically result in settlements exceeding $500,000, with averages often surpassing $1 million to cover lifelong care for conditions like cerebral palsy. Controversies surrounding perinatal asphyxia litigation include the overuse of the term "birth asphyxia" in lawsuits, which can oversimplify complex etiologies and promote claims based on outdated assumptions about neonatal distress. This misuse arises from misconceptions, such as equating routine needs with hypoxic damage, despite evidence that most low Apgar cases lack confirmed intrapartum oxygen deprivation. Legal standards have evolved since the widespread adoption of therapeutic hypothermia around 2005, which has become the for moderate to severe following , complicating retrospective assessments of by altering expected outcomes and requiring updated criteria for proving avoidable . The burden of proof in these cases heavily relies on expert testimony to establish the timing and preventability of the hypoxic insult, as plaintiffs must show by a preponderance of evidence that deviations from the directly caused the injury, though standards differ by (e.g., beyond in criminal cases). Qualified medical experts are essential for explaining how monitoring errors breached norms and linking them to specific outcomes, often using a of , timing, and liability to navigate the complexities of claims.

Forensic Considerations

Forensic investigations into perinatal asphyxia primarily involve detailed post-mortem examinations to establish the cause, timing, and circumstances of , distinguishing between acute intrapartum events and chronic antenatal insults. protocols emphasize comprehensive sampling of the and fetal/neonatal organs, with placental examination being crucial for identifying lesions associated with asphyxia, such as abruption or infarcts. Gross inspection includes measuring placental weight and dimensions, photographing surfaces, and sectioning to detect retroplacental hematomas indicative of abruption, which have a histological specificity of 100% but sensitivity of only 30.2%. Microscopic follows standardized guidelines, assessing for maternal vascular malperfusion through infarcts affecting more than 30% of the , which can signal chronic hypoxia leading to fetal compromise. Determining the timing of asphyxia relies on biochemical markers from cord blood and tissues, integrated into forensic analysis to differentiate acute from chronic events. Umbilical cord arterial blood gases, with a base deficit (BD) ≥12 mmol/L indicating intrapartum asphyxia and BD ≥20 mmol/L correlating with a 33% risk of cerebral palsy, provide objective evidence of metabolic acidosis onset, increasing approximately 0.5 mmol/L per minute during cord occlusion. Lactate levels in cord blood similarly reflect hypoxia severity, with elevations persisting due to minimal neonatal clearance in the first 1-2 hours post-delivery, aiding in pinpointing whether the insult occurred prenatally, intrapartum, or postnatally. These analyses complement histological timelines, such as early meconium-laden macrophages in the lungs appearing 1-6 hours after fetal distress, to reconstruct the sequence of events. Proper is essential in forensic perinatal cases, maintaining a strict for all samples to ensure evidentiary integrity, particularly when findings may influence criminal proceedings or claims. Protocols require sequential logging of sample collection, transfer, and analysis, including fresh placental tissues for and fixed blocks for , to prevent or degradation. In criminal cases, such as suspected involving , evidence like organ congestion, petechial hemorrhages, or meconium aspiration distinguishes natural intrapartum events from inflicted trauma, often corroborated by maternal history and scene investigation. These documented findings can support charges of or abuse if vital reactions, such as indicating live birth, are absent. For evaluations, they clarify as the primary cause versus contributing factors like . Adherence to established guidelines, such as those from the Royal College of Pathologists (RCPath), ensures standardized perinatal post-mortems, recommending multidisciplinary reviews involving pathologists, obstetricians, and neonatologists to interpret complex cases. RCPath protocols (e.g., G160) mandate , full-body , and targeted sampling for non-malformed fetuses dying antepartum or intrapartum, emphasizing placental and histology to exclude mimics of . These reviews, often through child death overview panels, integrate results with clinical records to refine cause-of-death statements, enhancing accuracy in medico-legal contexts. Such approaches may inform brief references to ensuing legal disputes, though the focus remains on evidentiary collection rather than litigation outcomes.

References

  1. https://www.ncbi.nlm.nih.gov/books/NBK430782/
  2. https://www.hopkinsmedicine.org/health/conditions-and-diseases/perinatal-asphyxia
  3. https://www.nature.com/articles/pr2017238
  4. https://www.mdpi.com/2227-9059/10/2/347
  5. https://www.who.int/teams/maternal-newborn-child-adolescent-health-and-ageing/newborn-health/perinatal-asphyxia
  6. https://pmc.ncbi.nlm.nih.gov/articles/PMC4737695/
  7. https://pmc.ncbi.nlm.nih.gov/articles/PMC8961792/
  8. https://publications.aap.org/pediatrics/article/117/4/1444/70944/The-Apgar-Score
  9. https://www.ncbi.nlm.nih.gov/books/NBK470569/
  10. https://www.researchgate.net/publication/320073281_From_Apparent_Death_to_Birth_Asphyxia_a_history_of_blame
  11. https://embryo.asu.edu/pages/apgar-score-1953-1958
  12. https://pmc.ncbi.nlm.nih.gov/articles/PMC9214735/
  13. https://www.frontiersin.org/journals/medicine/articles/10.3389/fmed.2022.944272/full
  14. https://pmc.ncbi.nlm.nih.gov/articles/PMC6491540/
  15. https://obgyn.onlinelibrary.wiley.com/doi/10.1111/aogs.14494
  16. https://www.frontiersin.org/journals/pediatrics/articles/10.3389/fped.2019.00489/full
  17. https://www.cambridge.org/core/books/fetal-and-neonatal-brain-injury/fetal-responses-to-asphyxia/964D0679006EC7CF6A423EFFFB3B67F0
  18. https://pmc.ncbi.nlm.nih.gov/articles/PMC3251192/
  19. https://www.cerebralpalsyguide.com/cerebral-palsy/causes/neonatal-asphyxia/
  20. https://pmc.ncbi.nlm.nih.gov/articles/PMC6390452/
  21. https://www.sciencedirect.com/science/article/pii/S0749073917303747
  22. https://www.uptodate.com/contents/meconium-aspiration-syndrome-pathophysiology-clinical-manifestations-and-diagnosis
  23. https://www.scirp.org/pdf/OJN_2016072915354488.pdf
  24. https://journals.sagepub.com/doi/10.1177/23779608241246874
  25. https://onlinelibrary.wiley.com/doi/10.1155/2020/4367248
  26. https://publications.aap.org/pediatrics/article/121/5/e1381/73446/Risk-Factors-for-Neonatal-Mortality-Due-to-Birth
  27. https://www.ucsfbenioffchildrens.org/-/media/project/ucsf/ucsf-bch/pdf/manuals/59_subabuse.pdf?rev=50983361dec94fffa54c32f74fc6533f
  28. https://www.merckmanuals.com/professional/pediatrics/perinatal-problems/small-for-gestational-age-sga-infant
  29. https://pubmed.ncbi.nlm.nih.gov/3361517/
  30. https://pmc.ncbi.nlm.nih.gov/articles/PMC8590025/
  31. https://pmc.ncbi.nlm.nih.gov/articles/PMC5719268/
  32. https://pubmed.ncbi.nlm.nih.gov/33186362/
  33. https://pmc.ncbi.nlm.nih.gov/articles/PMC2377391/
  34. https://www.cureus.com/articles/330246-birth-asphyxia-risk-factors-complications-and-outcomes-in-neonates-admitted-at-a-tertiary-care-center-in-gujarat-india
  35. https://doi.org/10.1007/s13760-020-01308-3
  36. https://pmc.ncbi.nlm.nih.gov/articles/PMC3171747/
  37. https://doi.org/10.1038/s41390-025-03978-2
  38. https://pmc.ncbi.nlm.nih.gov/articles/PMC10607511/
  39. https://pmc.ncbi.nlm.nih.gov/articles/PMC7670012/
  40. https://pmc.ncbi.nlm.nih.gov/articles/PMC5036328/
  41. https://pmc.ncbi.nlm.nih.gov/articles/PMC3740949/
  42. https://pubmed.ncbi.nlm.nih.gov/987769/
  43. https://jamanetwork.com/journals/jamaneurology/fullarticle/574959
  44. https://emedicine.medscape.com/article/973501-clinical
  45. https://pmc.ncbi.nlm.nih.gov/articles/PMC2675384/
  46. https://www.frontiersin.org/journals/neurology/articles/10.3389/fneur.2012.00144/full
  47. https://emedicine.medscape.com/article/973501-workup
  48. https://cpr.heart.org/en/resuscitation-science/cpr-and-ecc-guidelines/neonatal-resuscitation
  49. https://www.who.int/publications/i/item/9789241503693
  50. https://www.ncbi.nlm.nih.gov/books/NBK567714/
  51. https://www.rch.org.au/rchcpg/hospital_clinical_guideline_index/Therapeutic_hypothermia_in_the_neonate/
  52. https://publications.aap.org/pediatrics/article/133/6/1146/76110/Hypothermia-and-Neonatal-Encephalopathy
  53. https://www.nejm.org/doi/full/10.1056/NEJMoa0900854
  54. https://www.nejm.org/doi/full/10.1056/NEJMoa2119660
  55. https://publications.aap.org/neoreviews/article/24/12/e771/195847/Potential-Adjuncts-to-Therapeutic-Hypothermia-to
  56. https://obgyn.onlinelibrary.wiley.com/doi/10.1111/1471-0528.17816
  57. https://emedicine.medscape.com/article/973501-overview
  58. https://www.healthline.com/health/birth-asphyxia
  59. https://www.who.int/news-room/fact-sheets/detail/newborn-health
  60. https://www.medpharmres.com/archive/view_article?doi=10.32895/UMP.MPR.8.2.12
  61. https://pmc.ncbi.nlm.nih.gov/articles/PMC4988334/
  62. https://www.nature.com/articles/s41390-025-03978-2
  63. https://hopeforhie.org/hie-and-neonatal-seizures/
  64. https://pmc.ncbi.nlm.nih.gov/articles/PMC10631647/
  65. https://hopeforhie.org/the-state-of-neonatal-hie-a-10-year-review-of-global-trends/
  66. https://pmc.ncbi.nlm.nih.gov/articles/PMC11763856/
  67. https://www.mdpi.com/1648-9144/57/9/988
  68. https://pmc.ncbi.nlm.nih.gov/articles/PMC8650814/
  69. https://www.nature.com/articles/s41390-024-03261-w
  70. https://www.psychiatrictimes.com/view/neurological-complications-perinatal-asphyxia
  71. https://karger.com/neo/article/114/3/253/229485/MRI-Changes-in-the-Thalamus-and-Basal-Ganglia-of
  72. https://www.bmj.com/content/340/bmj.c363
  73. https://www.ijpediatrics.com/index.php/ijcp/article/download/5671/3480/24346
  74. https://pmc.ncbi.nlm.nih.gov/articles/PMC4117736/
  75. https://pmc.ncbi.nlm.nih.gov/articles/PMC9652677/
  76. https://hiehelpcenter.org/what-is-hypoxic-ischemic-encephalopathy/hie-facts-statistics/
  77. https://www.researchgate.net/publication/227934540_The_continuing_fall_in_incidence_of_hypoxic-ischaemic_encephalopathy_in_term_infants
  78. https://www.utsouthwestern.edu/newsroom/articles/year-2023/nov-newborn-boys-girls.html
  79. https://www.researchgate.net/publication/369690223_Associations_between_low_birth_weight_and_perinatal_asphyxia_A_hospital-based_study
  80. https://journals.lww.com/cmj/fulltext/9900/global%2C_regional%2C_and_national_burden_of_neonatal.1616.aspx
  81. https://pmc.ncbi.nlm.nih.gov/articles/PMC11863858/
  82. https://www.cdc.gov/group-b-strep/testing/index.html
  83. https://www.uptodate.com/contents/biophysical-profile-test-for-antepartum-fetal-assessment
  84. https://www.acog.org/clinical/clinical-guidance/clinical-consensus/articles/2025/04/tailored-prenatal-care-delivery-for-pregnant-individuals
  85. https://www.who.int/publications/i/item/WHO-RHR-18.02
  86. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0222566
  87. https://obgyn.onlinelibrary.wiley.com/doi/10.1016/j.ijgo.2015.06.020
  88. https://pmc.ncbi.nlm.nih.gov/articles/PMC9689968/
  89. https://www.sciencedirect.com/science/article/pii/S0301211524007139
  90. https://www.acog.org/clinical/clinical-guidance/clinical-practice-guideline/articles/2024/01/first-and-second-stage-labor-management
  91. https://srishtifertility.com/managing-cord-prolapse-to-prevent-birth/
  92. https://www.who.int/publications/i/item/9789240017566
  93. https://pmc.ncbi.nlm.nih.gov/articles/PMC6464257/
  94. https://obgyn.onlinelibrary.wiley.com/doi/10.1111/aogs.12276
  95. https://pubmed.ncbi.nlm.nih.gov/3399471/
  96. https://www.sciencedirect.com/science/article/pii/S0301211525009972
  97. https://www.sciencedirect.com/science/article/pii/S2090536X16300041
  98. https://www.lawfirm.com/birth-injury/birth-injury-settlements/
  99. https://pubmed.ncbi.nlm.nih.gov/34301500/
  100. https://www.justia.com/birth-injuries/birth-injury-lawsuits/expert-testimony-in-birth-injury-lawsuits/
  101. https://pubmed.ncbi.nlm.nih.gov/8075516/
  102. https://pmc.ncbi.nlm.nih.gov/articles/PMC8585837/
  103. https://pmc.ncbi.nlm.nih.gov/articles/PMC8069793/
  104. https://pmc.ncbi.nlm.nih.gov/articles/PMC6490584/
  105. https://www.rcpath.org/resourceLibrary/guidelines-on-autopsy-practice-fetal-autopsy-following-antepartum-or-intrapartum-death-of-non-malformed-fetuses.html
Add your contribution
Related Hubs
User Avatar
No comments yet.