The Journal of Maternal-Fetal and Neonatal Medicine, October 2009; 22(S3): 54–56

REVIEW

Neonatal asphyxia and forensic medicine

E. D’ALOJA, M. MÜLLER, F. PARIBELLO, R. DEMONTIS, & A. FAA

Forensic Science Department, Cagliari University, Monserrato, Cagliari, Italy

(Accepted 8 July 2009)

Abstract
In the last decades, the scientific literature addressing neonatal encephalopathy has grown in a logarithmic way and
malpractice claims in obstetrics and neonatology have become a major threat to the health service. At the moment, scientific
evidence are insufficient to clearly identify in each single case whether the hypoxic insult has developed in the course of labor
or in the first few hours after the birth or, otherwise, whether the damage has to recognize a remote and long-lasting cause
acting during pregnancy. Several authors feel that this scientific uncertainty leads to a higher percentage of civil suit decisions
prone to recognizing a guilty medical behavior, and they wish a more in-depth analysis of all these cases to clearly identify all
the data either in favor or in contrary to the assumption of the existence of a causal correlation between neonatal
encephalopathy and medical misbehavior. This article will focus on the medico-legal approach to a hypoxic–ischemic event
in the perinatal period, addressing the relevant data to be collected in order to establish the medical and juridical cause of the
neonatal damage.

Keywords: Neonatal asphyxia, forensic medicine, malpractice, diagnostic criteria, consensus statement

Although more and more reliable tools are routinely
employed during labor to assess the fetal well-being,
birth or intra-partum asphyxia remains a consider-
able problem in perinatal medicine with an incidence
ranging from 1 to 6 neonates every 1000 live full-
term births [1]. About 50% of these infants will
develop a hypoxic–ischemic encephalopathy (HIE)
and those with moderate (stage 2) to severe (stage 3)
HIE (according either to the Fenichel and the Sarnat
classification; [2,3]) are at high risk of developing
cerebral palsy (CP; [4]).
Recent data also suggest that intrapartum hypoxia
or asphyxia has to be considered as the third most
common cause of newborn death (23%) after
infections (36%) and preterm birth (28%) [5].
A large proportion of these events has been
considered ‘avoidable’ [6] or ‘preventable’ [7],
suggesting the hypothesis that a different medical
behavior could have led to the birth of a normal
infant.
From a juridical point of view, it has to be
considered that neonatal cerebral damages secondary
to intrapartum asphyxia are awarded with the highest
settlements (up to several million dollars/euros) in
the medical malpractice lawsuits scenario.
If those aspects are considered at once, the
significance of this issue in the medico-legal context
can be easily appraised.
In the last decades, several papers addressed to the
peripartum asphyxia mechanisms in order to identify
a clear-cut boundary between the prenatal and
perinatal causes and to share common criteria to
classify the CP cases. In spite of all the efforts, up to
now the major diagnostic criteria still rely on signs
and symptoms more than on objective issues.
Clinicians and forensic experts, acting as expert
witness in the court, sometimes feel confused with
the conditions of perinatal asphyxia, hypoxic–is-
chemic encephalopathy, neonatal encephalopathy
and CP due to the lack of a clear definition for each
term whenever employed, this topic having been
considered as the ‘Bermuda Triangle’ of neonatology
[8]. Furthermore, its timing, duration and outcomes
are poorly defined.
CP, as defined by the International Working Group
on Definition and Classification of Cerebral Palsy, is

Correspondence: E. d’Aloja. E-mail: ernestodaloja@medicina.unica.it

ISSN 1476-7058 print/ISSN 1476-4954 online Ó 2009 Informa UK Ltd.
DOI: 10.1080/14767050903198397
 Neonatal asphyxia and forensic medicine 55

a ‘group of permanent disorders of the development
of movement and posture, causing activity limitation,
that are attributed to non-progressive disturbances
occurred in the developing fetal or infant brain. The
motor disorders of CP are often accompanied by
disturbances of sensation, perception, cognition,
communication, and behavior, by epilepsy, and by
secondary musculoskeletal problems’ [9].
Intrapartum asphyxia is a condition that occurs
when there is an impairment of blood gas exchange,
resulting in hypoxemia and hypercapnia accompa-
nied by the development of metabolic acidosis [10].
Neonatal encephalopathy is a clinically defined
syndrome of disturbed neurologic function in the
earliest days of life in the term infant manifested by
difficulty with initiating and maintaining respiration,
depression of tone and reflexes, subnormal levels of
consciousness, and often by seizures [11].
If we focus our attention on the CP definition
criteria (representing the most interesting item for
medico-legal reason), we can observe several differ-
ences and similarities (depicted in Table I) in the last
three definitions proposed by International Scientific
Societies and Task Force.
Among the essential criteria for the diagnosis of CP,
the Apgar Score and the presence of multi organ
dysfunction (MODs) signs – initially considered as
mandatory for the diagnosis – have been discarded in
favour of a more stringent clinical manifestation of
the movement disability (only the spastic quadriplegia
and the dyskinetic type) and the clear exclusion of
other pathologies.
The cornerstone in all the definitions considered
so far has been the existence of a severe metabolic
acidosis grounded on the early detection – and
documentation – of a fetal blood pH 5 7.0 and a
base deficit 4¼ 12 mmol/L in an infant showing
precocious signs of moderate/severe encephalopathy.
According to these consensus statements, the lack
of one of these essential criteria is not only enough to
raise doubts on the existence of an intrapartum
damage, but also the alleged causal correlation
between severe metabolic acidosis and cerebral
damage has been questioned. Graham et al. [12]
reviewing several studies correlating an umbilical
arterial pH 5 7 to neonatal neurologic morbidity and
mortality stated that when using cord blood pH at
the time of birth, the incidence of having an
umbilical arterial pH 5 7 was 3.7 of 1000 term live
births, but only 23.1% of them had neonatal
neurologic morbidity or mortality.
In addition, the promising field of magnetic
resonance imaging (MRI) techniques – such as
diffusion tensor imaging (DTI) and proton magnetic
resonance spectroscopy – and biomarkers of brain
injuries investigation are not conclusive as yet.
Two major patterns of brain injury may be
detectable by MRI in the human term newborn with

Table I. Consensus statements on diagnosing intrapartum asphyxia.

American Academy of
Pediatrics/American
College of Obstetrics and International Cerebral Palsy American College of Obstetrics and
Gynecology (1996)* Task Force (1999){ Gynecology (2002){

Essential . Profound metabolic
criteria acidosis (pH 5 7.0)
. Apgar score 5¼ 3 after 5 min
. Neonatal encephalopathy
. Multi-organ system dysfunction
Additional
criteria
. Metabolic acidosis in early
neonatal blood sample
(pH 5 7 and base deficit
4¼ 12 mmol/L)
. Moderate or severe
encephalopathy
. CP of spastic quadriplegia
or dyskinetic type
. Sentinel event
. Abrupt change in foetal heart rate
. Apgar score 56 beyond 5 min
. Multi-system involvement
. Imaging evidence
. Metabolic acidosis (pH 5 7.0
and base deficit 4¼ 12 mmol/L)
. Moderate or severe encephalopathy
. CP of spastic quadriplegia
or dyskinetic type
. Exclusion of other pathologies of CP
. Sentinel event
. Abrupt change in fetal heart rate
. Apgar score 5¼ 3 beyond 5 min
. Multi-system failure within 72 h of life
. Imaging evidence

Biomarkers to be employed as early (before age 96 h) predictors of outcomes in full term neonates are:
. CSF Neuron Specific Enolase (NSE);
. CSF and Serum Interleukin 1 b;
. Serum Interleukin 6;
. S100b.
Although promising, none of these biomarkers have been so far implemented into the routine clinical use.
*Committee on Fetus and Newborn, Committee on Obstetric practice. Use and Abuse of the Apgar Score. Pediatrics 1996;98(1):141–142.
{
MacLennan A. A template for defining a causal relation between acute intrapartum events and CP: International Consensus Statement.
BMJ 1999;319(7216):1054–1059.
{
Task Force American College of Obstetricians and Gynecologists and The American Academy of Pediatrics. Neonatal encephalopathy and
CP. Defining the pathogenesis and pathophysiology. Washington DC, ACOG, 2003.
56 E. d’Aloja et al.
encephalopathy [13]. The watershed predominant
pattern seems to be related to a prolonged asphyxia
and involves the white matter and may extend
toward the gray matter if the insult is severe enough.
The basal nuclei predominant pattern represents acute
profound asphyxia with gray matter predominant
involvement.
Different evidence might come from the study of
biomarkers related to the hypoxic insult [14].
Although several promising molecules have been
described (such as S100b, serum/CSF interleukin-
1b, serum interleukin-6 and CSF NSE), no routine
use of such markers has been up to now implemen-
ted into the clinical setting.
Uncertainty seems to be the only shareable data in
the clinical context.
But if we transfer this ambiguity to the juridical
arena, the presence of a pH 4 7.0 with a base
deficit 4¼ 12 mmol/L can be used as a sound evi-
dence to state that the origin of the cerebral damage
cannot be identified in a peripartum hypoxic event, but
has to recognize a different origin in a clinical period
when neither the gynecologist nor the neonatologist
could act in any way to avoid such a damage. On the
other hand, a severe metabolic acidosis at the time
of birth or shortly after it, in the absence of other
demonstrable cause of brain lesion, is going to be
accepted as the reliable proof of a fetal distress during
the labor or the first few hours supporting the
hypothesis of a medical malpractice.
In a judicial system as the Italian Civil one where
physicians have to prove that their behavior was
correct and that no breach of duty occurred during
the infant’s medical assistance, being unable to
identify the cause of the cerebral damage may let
the judge rule in favor of the plaintiff and against the
physicians.
For this reason, a CP claim requires the physician
to provide all the available data, especially those
related to other possible causative explanations of
the brain damage or those excluding that the
hypoxic–ischemic event occurred during the perina-
tal period.
Declaration of interest: The authors report no
conflicts of interest. The authors alone are respon-
sible for the content and writing of the paper.
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