Important Facts about Cerebral Palsy

ACOG: Neonatal Encephalopathy & CP: Defining the Pathogenesis & Patholophysiology 2003)

In 1999, the International Cerebral Palsy Task Force composed of obstetricians, neonatologists, child neurologists and other specialties developed criteria that define a relationship between intrapartum events and cerebral palsy. An AGOG Task Force, working with the American Academy of Pediatrics, updated the criteria early in 2003.

Key Points:

Cerebral palsy occurs as a result of intrapartum events in only 10 percent of cases. Only cerebral palsy involving spastic quadriplegia is associated with acute interruption of the blood supply; purely dyskinetic or ataxic cerebral palsy is usually genetic in origin. Prematurity, and thus multiple pregnancies, have a causal relationship to cerebral palsy. Cerebral palsy has many causes including developmental abnormalities, metabolic anomalies, infection, coagulation disorders, autoimmune disorders, trauma, antepartum events such as temporary cord occlusion, and intrapartum events. Neonatal acidemia may represent difficult or ineffective resuscitation rather than asphyxia.

There are four essential conditions that must be met in order to define an intrapartum event as sufficient to cause cerebral palsy:

• Metabolic acidosis (ph <7 and base deficit of 12)
  
  
• Early onset of moderate to severe neonatal encephalopathy at 34 or more weeks
  
  
• Spastic quadriplegia or dyskinetic type of cerebral palsy
  
  
• Exclusion of factors such as trauma, coagulation disorders, infection or genetic disorders.
  

Taken collectively, the following are suggestive but nonspecific factors related to cerebral palsy:

• Recognized sentinel event such as abruption
  
  
• Sudden and sustained bradycardia or absence of variability in presence of persistent late decelerations or non-reassuring variable decelerations when the tracing was previously normal
  
  
• Apgar scores of 0-3 beyond five minutes, onset of multisystem involvement within 72 hours of birth
  
  
• Early imaging studies showing evidence of acute nonfocal cerebral pathology

Think of antepartum events, or sleep cycle or medications, when the patient presents with fetal tracing showing decreased variability. Fetal monitoring is not for fetal well being, it is for perfusion. Except for an unequivocally reassuring strip or perhaps a strip showing absent variability in presence of persistent late decelerations/ bradycardia/nonreassuring variables, there is wide interpretation among clinicians and so-called experts as to appropriateness of actions taken or not taken.

Document sentinel events (hypoxemic events occurring immediately before or during labor such as abruption, uterine rupture, hypotension) and look for cord occlusion evidence (true knot) and abruption evidence when a poor outcome occurs. Complete placental abruption, when it occurs immediately prior to delivery, is difficult to diagnose but may be a factor.

Page 1: Fetal Monitoring and Related Delivery Decisions
Page 2: Important Facts about Cerebral Palsy
Page 3: Oxytocin, History of Cesarean Section/VBAC, Group B Streptococci Carriers
Page 4: Shoulder Dystocia, Placental Pathology, Documentation & Records