B10. Disturbances of the feto-maternal gas transport during labor

From greek.doctor

Perinatal asphyxia refers to the condition in which foetal gas exchange is abnormal antepartum, intrapartum, or postpartum, which leads to the neonate’s brain and other organs being deprived of oxygen. It’s characterised by progressive hypoxaemia, hypercarbia, and lactic acidosis. Unless reversed, perinatal asphyxia will cause irreversible CNS damage and other organ damage, or even death.

The main complication of perinatal asphyxia is hypoxic-ischaemic encephalopathy (HIE), although injury to organ system like heart, kidney, lung, and liver are also common. The long-term outcome of HIE is often cerebral palsy.

Perinatal asphyxia is a major cause of foetal death worldwide, especially in developing countries.

Etiology

Perinatal asphyxia is caused by a hypoxic or ischaemic event occurring immediately before or during labour. The list of possible causes is long:

  • Uterine rupture
  • Placental abruption
  • Umbilical cord prolapse
  • Amniotic fluid embolism
  • Vasa praevia
  • Foetomaternal haemorrhage

Many risk factors increase the risk of developing perinatal asphyxia in the setting of one of the events listed above. These include risk factors which decrease the adaptability of the mother, placenta, and foetus, including:

  • Foetal prematurity, congenital heart defect
  • Placental abnormalities
  • Maternal diabetes, heart failure, preeclampsia

Pathomechanism

The foetus responds to perinatal asphyxia by redistributing blood flow from nonvital organs to the brain and heart. As such, if hypoxic-ischaemic injury of the brain and heart has occurred, injury to nonvital organs is very likely. Hypoxia severe enough to cause myocardial dysfunction will lead to decreased cardiac output and worsening ischaemia of end-organs.

Clinical features

Typical signs and symptoms of perinatal asphyxia include:

  • Apgar score < 5
    • Especially cyanosis, bradycardia, decreased muscle tone
  • Acidosis (pH < 7) or base deficit > 12 mM (determined from arterial umbilical cord blood or normal venous blood)
  • MRI-findings indicating hypoxic-ischaemic CNS injury
  • Signs of multi-organ failure
    • Acute kidney injury -> oliguria, increased serum creatinine
    • Heart injury -> reduced CO, hypotension
    • Neonatal respiratory distress -> respiratory insufficiency
    • Hepatic effects -> liver enzyme elevation, hypoalbuminaemia
    • Gastrointestinal effects -> reduced tolerance of enteral feeding
    • Haematological effects -> DIC

Diagnosis and evaluation

The diagnosis is made based on typical clinical features in the context of a peripartum event which could cause perinatal asphyxia (see etiology). Pathological intrapartum CTG findings (bradycardia, variable/late decelerations, absent variability, sinusoidal wave) are also present.

If the diagnosis is made or suspected, several investigations may be made:

  • Blood gas analysis (for acid-base status)
  • CBS (for infection, haemorrhage, thrombocytopaenia)
  • Liver function tests (for possible injury)
  • Kidney function tests (for possible injury)
  • Cardiac enzymes (for possible injury)
  • Coagulation tests (for DIC)
  • Blood culture (to exclude sepsis)
  • EEG

MRI is the most sensitive tool for distinguishing hypoxic-ischaemic CNS injury from other causes of neonatal encephalopathy.

Treatment

Perinatal asphyxia is usually suspected before the foetus itself is delivered, based on the presence of a peripartum event and pathological CTG findings. In these cases, measures and personnel required for neonatal resuscitation should be readied.

Following birth, the neonate requires resuscitation and stabilisation (topic B12).

Therapeutic hypothermia is the only measure which improves the prognosis of perinatal asphyxia and hypoxic-ischaemic encephalopathy. It refers to reducing the body temperature to 33 – 34°C, which protects the brain and other organs. Therapeutic hypothermia must wait until after resuscitative measures have stabilised the neonate but must be applied no more than 6 hours after birth. The inclusion criteria are (all must be present):

  • Gestational age > 36 weeks
  • Clinical diagnosis of moderate to severe encephalopathy
  • Any of the following
    • Signs of acidosis (pH < 7, base deficit > 16 mM)
    • 10-minute Apgar score of 5 or less
    • Ongoing resuscitation initiated at birth and continued for 10 minutes

Complications

The most frequent long-term complications are CNS-related.

  • Cerebral palsy
  • Epilepsy
  • Abnormal intellectual development

Prognosis

Despite the development of severe complications peripartum, full recovery is possible, especially with the proper use of therapeutic hypothermia. However, in most cases of moderate or severe encephalopathy, long term CNS complications manifest. Of those infants affected, 15-20% die in the neonatal period, and up to 25% of survivors are left with permanent neurologic deficits.