ASPHYXIA NEONATORUM PATHOPHYSIOLOGY PDF

The highest score possible is A baby with a lower Apgar score after 5 minutes has a higher risk for asphyxia neonatorum. The doctor may suspect your baby has asphyxia neonatorum if they have an Apgar score of 3 or lower for more than 5 minutes. This can indicate poor oxygenation.

Author:Fenrikazahn Fenrigul
Country:Portugal
Language:English (Spanish)
Genre:Career
Published (Last):18 January 2005
Pages:233
PDF File Size:2.92 Mb
ePub File Size:16.74 Mb
ISBN:590-2-88529-399-5
Downloads:24892
Price:Free* [*Free Regsitration Required]
Uploader:Vurn



Received Apr 29; Accepted May Abstract Perinatal asphyxia occurs still with great incidence whenever delivery is prolonged, despite improvements in perinatal care. After asphyxia, infants can suffer from short- to long-term neurological sequelae, their severity depend upon the extent of the insult, the metabolic imbalance during the re-oxygenation period and the developmental state of the affected regions.

Significant progresses in understanding of perinatal asphyxia pathophysiology have achieved. However, predictive diagnostics and personalised therapeutic interventions are still under initial development. Now the emphasis is on early non-invasive diagnosis approach, as well as, in identifying new therapeutic targets to improve individual outcomes.

In this review we discuss i specific biomarkers for early prediction of perinatal asphyxia outcome; ii short and long term sequelae; iii neurocircuitries involved; iv molecular pathways; v neuroinflammation systems; vi endogenous brain rescue systems, including activation of sentinel proteins and neurogenesis; and vii therapeutic targets for preventing or mitigating the effects produced by asphyxia.

Keywords: Neonatal, Hypoxia-ischemia, Predictive diagnostic, Sequelae, Personalised treatments Introduction Perinatal asphyxia PA or neonatal hypoxia- ischemia HI is a temporary interruption of oxygen availability that implies a risky metabolic challenge, even when the insult does not lead to a fatal outcome [ 1 ]. The staging system proposed by Sarnat and Sarnat in is often useful in classifying the degree of encephalopathy.

Mild stage I , moderate stage II , or severe stage III HIE is commonly diagnosed using physical examination, which evaluates the level of consciousness, neuromuscular control, tendon and complex reflexes, pupils, heart rate, bronchial and salivary secretions, gastrointestinal motility, presence or absence of myoclonus or seizures, electroencephalography findings, and autonomic function [ 4 ].

However, these parameters have no predictive value for long-term neurologic injury after mild to moderate asphyxia [ 5 ]. PA is a major paediatric issue with few successful therapies to prevent neuronal damage. PA still occurs frequently when delivery is prolonged, despite improvements in perinatal care [ 6 — 9 ]. Prognosis and sequelae of perinatal asphyxia Studies of neurodevelopmental outcome after HIE often give limited information about the children, pooling a wide range of outcome severities.

The emphasis in neonatology and paediatrics is on non-invasive diagnosis approaches for predictive diagnostics. Several methods for predicting outcomes in infants with HIE are used in the clinical setting including: neonatal clinical examination and clinical course, monitoring general movements [ 15 , 16 ], early electrophysiology testing, cranial ultrasound imaging, Doppler blood flow velocity measurements, magnetic resonance imaging MRI and MR microscopy.

The neonatal brain MRI provides detailed information about lesion patterns in HIE allowing for earlier and more accurate prediction of long-term outcome [ 17 , 18 ]. Very recently, a potential serum biomarker for predicting individual predispositions to pathologies or progression of complications induced by asphyxia has been described.

As HIE induces changes in blood-barrier permeability [ 19 ], a potential correlation between blood and brain can be established. This result is of clinical interest offering a potential inexpensive and safe prognostic marker for newborn infants with PA. Long-term follow-up studies are required to correlate the information obtained from early biomarkers predictor with clinical-pathophysiologic outcome. The time course and the severity of the neurological deficits observed following HI depends upon the extent of the insult, the time lapse before normal breathing is restored and the CNS maturity of the foetus.

Severe asphyxia has been linked to cerebral palsy, mental retardation, and epilepsy [ 7 , 21 — 23 ], while mild-moderate asphyxia has been associated with cognitive and behavioural alterations, such as hyperactivity, autism [ 22 ], attention deficits in children and adolescents [ 24 , 25 ], low intelligence quotient score [ 26 ], schizophrenia [ 27 — 29 ] and development of psychotic disorders in adulthood [ 30 ].

In a prospective cohort study of genetic and perinatal influences on the aetiology of schizophrenia [ 26 , 31 ], it was reported that individuals with hypoxia-related obstetric complications were more than five times more likely to develop schizophrenia than individuals with no hypoxia-related obstetric complications. Moreover, a downregulation of brain-derived neurotrophic factor BDNF has been detected in cord samples of patients exposed to PA who develop schizophrenia as adults [ 27 ].

This finding suggests that the decrease in neurotrophic factors induced by HI may lead to dendritic atrophy and disruption of synaptogenesis, effects that are present in individuals destined to develop schizophrenia as adults [ 27 ].

Moreover, in a year longitudinal study, it was found that neonatal HI complications were associated with a doubling of the risk for developing a psychotic disorder [ 32 ]. Because the majority of studies have focused on detecting major developmental abnormalities at a very young age, we still know little about the less severe difficulties that children may experience later, since different levels of morbidity have been found after mild or moderate PA [ 33 ].

To understand the long-term effects of PA on development, it is necessary to follow participants through school age. Specific cognitive functions continue to develop throughout childhood, and subtle functional deficits usually become apparent when a child faces increasing demands to develop complex abilities in school. Given the good prognosis of children with mild PA, the heterogeneity of moderate PA, and the devastating effects of severe PA, some authors have proposed a dose—response effect [ 9 , 37 ].

Neurocircuitries of the hippocampus, as well as the basal ganglia [ 10 , 24 , 39 — 43 ], are particularly vulnerable to HI in the neonate [ 18 , 44 — 50 ]. Hippocampus have been associated with specific cognitive functions such as memory and attention and together with striatum, play a role in the pathogenesis of attention deficit hyperactivity disorder, autism and schizophrenia [ 10 , 51 , 52 ].

The striatum has also been associated with cerebral palsy, a group of disorders of movement and posture development. This group also shows increased susceptibility for developing cerebral palsy, including athetosis and dystonia, with impaired motor speech and impaired use of the hands compared to the legs [ 54 ]. The early MRIs showed marked structural damage to the deep grey matter, hippocampus, or frontal white matter, producing a long-term impact on intellectual function in the children.

Language problems were also common [ 17 ]. These MRI findings provide evidence of the close relationship between the localisation of the lesion, the severity of the HI injury, and the resulting functional impairment.

A similar system-selective pattern of network degeneration in the hippocampus has been seen with diffusion tensor MRI in mice with hypoxic-ischaemic injury [ 55 , 56 ]. Moreover, a decrease in synaptogenesis and dendritic branching of pyramidal cells has been found in hippocampal cultures from rats exposed to PA [Rojas-Mancilla et al.

These effects could be correlated with deficits in neuro-behavioural functions such as hyperactivity, deficits in working memory, non-spatial memory, anxiety, and motor coordination [ 40 , 42 , 61 , 63 , 64 — 66 ] and also could be a key factor in the development of neuropathology, including schizophrenia [ 27 ].

EUDOCIMUS RUBER PDF

Asphyxia Neonatorum

For the more general term covering inadequate oxygen supply to the fetus, see intrauterine hypoxia. Perinatal asphyxia Pediatrics , obstetrics 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 is also the inability to establish and sustain adequate or spontaneous respiration upon delivery of the newborn. It remains a serious condition which causes significant mortality and morbidity.

100 PESAN NABI UNTUK WANITA SOLEHAH PDF

Pathophysiology of perinatal asphyxia: can we predict and improve individual outcomes?

.

CARCINOMA BRONCOGENICO PDF

Pathophysiology of Birth Asphyxia.

.

DIFFERENTIAL MANIFOLDS KOSINSKI PDF

Perinatal asphyxia

.

Related Articles