INTRODUCTION:
Perinatal asphyxia newborn futures remains a public health problem in developing countries, given the morbidity and mortality it causes.
It is the most frequent cause of damage to the central nervous system of perinatal origin.
Its incidence varies according to the health status of countries according to the quality of obstetric teams.
His estimate remains difficult to assess due to the problems of definition of perinatal asphyxia that hinder the realization of large-scale epidemiological studies.
EPIDEMIOLOGY:
The incidence remains high, estimated at 2-4 / 1000 births by 1995 in the Thorenberg suédoire population.
HAGBERG. B reported an incidence of 4-9 per 1000 births in Sweden.
It is estimated at 2 cases / 1000 live births by 2000 in the IWRM French population.
BADAWI reported an incidence of 2-8 per 1000 live births.
MING Chiali reported an incidence of 1-3 cases per 1000 births.
Prof. HARIDI reported in his thesis 11% of cases of neonatal asphyxia among the 550 newborns hospitalized each year. During 2011, there was in Beni Messous 80 infants hospitalized for neonatal asphyxia among 12,000 live births.
This incidence is unchanged despite advances in perinatal medicine. Childbirth thus keeping a share of hardly avoidable risks.
Fetal distress complicates 1.5% das deliveries.
Neonatal encephalopathy is estimated at 2-8 / 1000.
10-20% of BMI were due to fetal distress.
Cerebral palsy affects 2-2.5 per 1000 live births.
The overall prognosis of neonates with asphyxia has hardly improved these past 20 years: about 1/3 of deaths, often heavy consequences 1/3, 1/3 survival without sequelae.
DEFINITIONS:
The American Academy of Pediatrics defines the hypoxic-ischemic encephalopathy by the association:
– APGAR score of <3 to 5 min.
– Umbilical acid pH.
– Early neurological distress.
– Multiple organ failure.
In 2002, the American College of Obstetrics and Gynecology adds the essential criteria: the existence of cerebral palsy spastic quadriplegia type or dyskinesia and exclusion of other causes. Other criteria suggest intrapartum anoxia with presence:
– A sentinel event (uterine rupture, retro placentae, eclampsia, cord prolapse, the last head retention).
– Abrupt change of Fetal Heart Rate (FHR).
– Specific MRI imagery.
Pathophysiology:
Faced with anoxia, the newborn uses several compensation phenomena to overcome this critical situation, with redistribution of blood volume to the noble organs (CNS Central Nervous System ++).
When these mechanisms are overwhelmed, anoxia may have adverse effects on all organs leading to multiple organ failure, the largest being the brain damage with subsequent neurological sequelae.
There are several phases in the genesis of neonatal encephalopathy:
1. Pre-asphyxial condition: such intrauterine growth failure, abnormal maternal metabolic state, viral foetapathie, post-maturity …
2. Phase of anoxia with reduction in energy intake, sodium entry and water, accumulation of calcium and neurotransmitters responsible for early neuronal death.
3. Phase of neuronal depression with normal energy level but a depressed neural activity associated with a release of free radicals and nitric oxide secondary to oxidative stress triggered by the phenomenon of reperfusion.
4. Phase of secondary delayed cell death of microvessel dysfunction and glutamatergic excitotoxicity by accumulation of calcium.
These phases suggest that there is a therapeutic window of a few hours (6 hours for most authors) for which an intervention is possible to prevent some of the brain damage.
CLINIC:
– Neurological disorders: are classified according to the severity according to the stages of Sarnat and Sarnat:
. Stage I: hyperexcitability, normal tone and primitive reflexes, sympathetic autonomic disorders (mydriasis, tachycardia, moderate congestion).
. STAGE II: depression of consciousness, muscle tone disorders, low or ABSCENTS primitive reflexes, autonomic parasympathetic signs (miosis, bradycardia, bronchial congestion, diarrhea), focal or multifocal seizures.
. STAGE III: coma, global hypotonia, lack of primitive reflexes, autonomic signs, status epilepticus or not décéréberation signs.
In addition to neurological disorders there are signs of multiple organ failure:
– Respiratory: respiratory distress secondary to meconium aspiration meconium knowing that is toxic to the air shaft.
– Cardiac: the risk of heart failure.
– Hepatic: with elevated liver enzymes and extreme liver failure.
– Renal: announcing with oliguria renal failure, and possible hematuria and proteinuria signing the glomerular disease.
– Intestinal: with the risk of ulcerative enterocolitis.
– Haemostasis: with risk of Disseminated Intravascular Coagulation (DIC).
FURTHER EXPLORATIONS:
1. Electroencephalography (EEG):
Examination of high prognostic value, requires a rigorous technical recording and an experienced player.
Allest revised EEG criteria to characterize the severity of neonatal encephalopathy:
– Normal or subnormal in EEG encephalopathy hypoxic-ischemic attack (EHI) Stage I.
– GET intermediate, continuous low voltage (5-25 uV) slow or intermittent continuous type A or B in the satde II.
– It is low voltage with theta rhythm, paroxysmal, periodic or inactive <5 uV in satde III.
2. Ultrasound trans fontanellaire:
It helps eliminate other causes of cerebral distress she may find periventricular échogénécités and lesions of the basal ganglia.
It can find indirect evidence of cortical atrophy.
3. MRI:
Performed within 15 days of preference. The most commonly used classification is that of MRI Baenziger:
Guy: Hyper diffuse signal (T1) of the 2 hemispheres with no differentiation SB / SG indicating extensive damage.
Type b: Hyper para sagittal signal (T2) to the junction of the middle cerebral artery, anterior and posterior.
Type c: hyper or hypo signal in the basal ganglia.
Type: periventricular leukomalacia.
E Type: localized ischemic or hemorrhagic stroke.
Type f: hypo-linear signals (T2) in the periventricular centrifugal semi oval center and the white matter of the frontal and occipital lobes.
etiologies:
1. dynamic dystocia:
– Hypersystolie more important and prolonged contractions with intensity> 60 mm Hg.
– Tachysystole: the frequency of contractions is greater than 5 per 10 minutes.
– Hypertonia: corresponds to a basic tone greater than 11 mm Hg in early labor and greater than 18 mm Hg at the end of work.
2. A working trio along depletes oxygen reserves.
3. Maternal causes: preeclampsia, diabetes, prolonged pregnancy that, complications of general anesthesia.
4. adnexal causes: retro-placental hematoma, placenta previa, chorioangioma, postion accidents cord (prolapse, tight circular).
5. Fetal causes: hyptorphie, macrosomia, prematurity, post-maturity, acute fetal anemia.
SUPPORTED :
Two therapeutic areas:
– Neuroressussitation.
– Neuroprotection.
goals
– Fight against edema.
– Maintains a cerebral perfusion pressure (CPP) correct.
– Avoid discomfort venous return.
a. Head Position:
head straight, surrélevée 30 ° to promote venous return.
b. Fluid restriction:
– 2/3 of normal needs maintains (60 cc / kg serum glucose SG 10%).
– Monitoring of weight, urine output and serum electrolytes.
– Maintenance of blood pressure (BP) Normal:
* Avoid sudden fluctuations in BP.
* Corrections conditions that may lead to abolition of the regulation of cerebral blood flow: hypoxia, hypercapnia, hypoglycaemia.
c. Treatment of seizures:
– Phenobarbital: Bulb: 40 mg = 1 cc.
* Attack Treatment: 20 mg / kg by slow intravenous (IVL) diluted in isotonic saline (ISS), renewable dose not exceeding 40mg / kg / day.
* Maintenance treatment: 3-5 mg / kg / day, 24 hours after the loading dose (DA).
* Side effects: drowsiness, hypotonia.
d. Controlled hypothermia: its protective effect is linked to:
– Reduction of the release of excitatory amino acids,
– Decrease in the synthesis of nitric acid,
– Decreased cerebral energy consumption.
It can be physical or selective (head) should be started between 6 and 72, the target temperature: 33-35 degrees.
Numerous studies have demonstrated improved neurological outcome of infants receiving this neuro-protection.
PROGNOSIS :
The elements of the prognosis:
Convulsions:
– Seizures are among the moderate and severe forms of l4EHI and may be indicative of poor prognosis.
– It is a poor prognostic marker, with risk of death by 33% during the first year and a risk of motor disability of 55% among survivors.
– Their early indicator is a derogatory and crises that occur before four hours of life are associated with adverse developments.
Immediate clinical course:
The speed of the return to normal is one of the key elements of the prognosis.
When a review is normalized during the first week of life this is generally associated with a favorable outcome against by an abnormal exam is associated with a poor prognosis significantly after 14 days of life.
Electroencephalogram (EEG):
This is an excellent prognostic tool, indeed: between the 12th and the 24th hour, the presence of significant abnormalities bottom trace is consistently associated with a poor outcome (death or serious sequelae).
Conversely, the normality of the plot is a good prognosis.
The monitoring of changes based on repeated clinical examinations, or even daily in the acute phase.
The child will be reviewed quarterly during the first year or better at key ages of psychomotor development to education to early detection of neuro-developmental abnormalities and support them effectively.
Such consultations shall be multidisciplinary.
PREVENTION:
Prenatal care:
– Monitoring quality of all pregnancy: this will allow the screening of high-risk pregnancies.
– Creation of a support center for high-risk pregnancy with personnel and equipment.
– Improved support (PEC) in the delivery room: it is imperative that maternity shall have in place:
* Cardio-tocographes: monitoring during labor of heart activity and uterine dynamics.
It must be systematic for all risk pregnancies.
And for the primipara, it is desirable that work rooms can have:
* PH meter to be able to monitor the pH in deliveries at high risk of suffering and the appearance of abnormal Fetal Heart Rate (FHR).
* Ultrasound to make emergency ultrasound, especially among women not followed, never having had previous ultrasounds.
Getting postnatal load:
– Staff training: the resuscitation of the newborn must be demystified. The principles and techniques must beings disseminated to all qualified workers in the labor room.
Indeed, for the successful birth of a newborn, a pédiare, an anesthesiologist or other person trained and driven, must be available at any time of the day to resuscitate the newborn if necessary.
– Preparation of resuscitation:
All work room must include a resuscitation room of the newborn with the materials and equipment necessary to ward off the worst of disasters.
At least 2 persons trained to be available well before the birth of the newborn to take cognizance of the parent folder.
In fact, communication between the obstetrician and pediatrician during work or before a cesarean delivery is a guarantee of success of resuscitation.
