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In his editorial, Freeman acknowledges the complexity of the issue and allows that some cases of CP are clearly caused by substandard intrapartum care, but he leaves many essential questions unanswered.1 Similarly, the meta-analysis itself offers multiple explanations of the possible causes of CP but relatively few conclusions that can be applied to any specific case of CP, when the cause in that case is unclear.
Authors focus on cord pH below 7.0
To be sure, an umbilical artery pH of less than 7.0 at birth is concerning, but even at this level of acidosis, results are conflicting. Combining data from multiple studies, the authors concluded that the incidence of significant neonatal neurologic morbidity and mortality was significant among nonanomalous infants who had such a pH level (23.1%). However, the remaining 76.9% of infants were neurologically normal at the time of hospital discharge.
Nor did Apgar scores predict asphyxial complications when cord pH was less than 7.0. However, the combination of an Apgar score of 3 or less and cord pH below 7.0 was a sensitive predictor of serious neonatal morbidity.
Questions abound—but not answers
It was thought that electronic fetal monitoring would eliminate intrapartum stillbirth and reduce the incidence of CP—but neither goal has been achieved. Moreover, the presence of meconium, long associated with nonreassuring fetal status, was found in one study to have no association with CP.2
As for the role of infection, inflammation, and intrapartum fever, Eastman and DeLeon suggested as early as 1955 that intrapartum fever was seven times more likely in mothers of children who were later diagnosed with CP than in mothers of normal children—and intrapartum fever, infection, and neonatal fever remain prime suspects in the CP mystery.3
How does the average clinical obstetrician interpret and use these results? How does our legal system use these results?
It depends. The overwhelming majority of nonanomalous term infants do well. For the few who develop CP, there often is an accepted reason for the diagnosis.
Graham and colleagues conclude that only 14.5% of CP cases are associated with intrapartum asphyxia. The dilemma? For that 14.5%—or even the remaining 85.5%—our ability to determine the true cause of CP in any given case is unreliable. Who or what test can conclusively eliminate intrapartum asphyxia as a medically probable cause?
The answers are disheartening.
- Recognize that prematurity and infection are the leading risk factors for cerebral palsy (CP) in nonanomalous infants.
- Be cognizant of the lack of predictive value—both positive and negative—of current methodologies, such as Apgar score and pH level, in regard to CP.
- Remember that neither the introduction of electronic fetal monitoring nor the increase in the cesarean delivery rate from 5.5% in 1970 to 31.1% in 2006 has appreciably altered the rate of CP in the United States.
- Don’t discount the importance of the first 20 minutes of postnatal life. They are perhaps at least as important as the final 20 minutes of fetal life. When delivering a patient who has a risk factor for CP, do not hesitate to request the presence of a skilled neonatologist for assistance with newborn resuscitation.—JOHN T. REPKE, MD
1. Freeman RK. Medical and legal implications for necessary requirements to diagnose damaging hypoxic–ischemic encephalopathy leading to later cerebral palsy. Am J Obstet Gynecol. 2008;199:585-586.
2. Nelson KB, Grether JK. Potentially asphyxiating conditions and spastic cerebral palsy in infants of normal birth weight. Am J Obstet Gynecol. 1998;179:507-513.
3. Eastman NJ, DeLeon M. The etiology of cerebral palsy. Am J Obstet Gynecol. 1955;69:950-961.
In his editorial, Freeman acknowledges the complexity of the issue and allows that some cases of CP are clearly caused by substandard intrapartum care, but he leaves many essential questions unanswered.1 Similarly, the meta-analysis itself offers multiple explanations of the possible causes of CP but relatively few conclusions that can be applied to any specific case of CP, when the cause in that case is unclear.
Authors focus on cord pH below 7.0
To be sure, an umbilical artery pH of less than 7.0 at birth is concerning, but even at this level of acidosis, results are conflicting. Combining data from multiple studies, the authors concluded that the incidence of significant neonatal neurologic morbidity and mortality was significant among nonanomalous infants who had such a pH level (23.1%). However, the remaining 76.9% of infants were neurologically normal at the time of hospital discharge.
Nor did Apgar scores predict asphyxial complications when cord pH was less than 7.0. However, the combination of an Apgar score of 3 or less and cord pH below 7.0 was a sensitive predictor of serious neonatal morbidity.
Questions abound—but not answers
It was thought that electronic fetal monitoring would eliminate intrapartum stillbirth and reduce the incidence of CP—but neither goal has been achieved. Moreover, the presence of meconium, long associated with nonreassuring fetal status, was found in one study to have no association with CP.2
As for the role of infection, inflammation, and intrapartum fever, Eastman and DeLeon suggested as early as 1955 that intrapartum fever was seven times more likely in mothers of children who were later diagnosed with CP than in mothers of normal children—and intrapartum fever, infection, and neonatal fever remain prime suspects in the CP mystery.3
How does the average clinical obstetrician interpret and use these results? How does our legal system use these results?
It depends. The overwhelming majority of nonanomalous term infants do well. For the few who develop CP, there often is an accepted reason for the diagnosis.
Graham and colleagues conclude that only 14.5% of CP cases are associated with intrapartum asphyxia. The dilemma? For that 14.5%—or even the remaining 85.5%—our ability to determine the true cause of CP in any given case is unreliable. Who or what test can conclusively eliminate intrapartum asphyxia as a medically probable cause?
The answers are disheartening.
- Recognize that prematurity and infection are the leading risk factors for cerebral palsy (CP) in nonanomalous infants.
- Be cognizant of the lack of predictive value—both positive and negative—of current methodologies, such as Apgar score and pH level, in regard to CP.
- Remember that neither the introduction of electronic fetal monitoring nor the increase in the cesarean delivery rate from 5.5% in 1970 to 31.1% in 2006 has appreciably altered the rate of CP in the United States.
- Don’t discount the importance of the first 20 minutes of postnatal life. They are perhaps at least as important as the final 20 minutes of fetal life. When delivering a patient who has a risk factor for CP, do not hesitate to request the presence of a skilled neonatologist for assistance with newborn resuscitation.—JOHN T. REPKE, MD
In his editorial, Freeman acknowledges the complexity of the issue and allows that some cases of CP are clearly caused by substandard intrapartum care, but he leaves many essential questions unanswered.1 Similarly, the meta-analysis itself offers multiple explanations of the possible causes of CP but relatively few conclusions that can be applied to any specific case of CP, when the cause in that case is unclear.
Authors focus on cord pH below 7.0
To be sure, an umbilical artery pH of less than 7.0 at birth is concerning, but even at this level of acidosis, results are conflicting. Combining data from multiple studies, the authors concluded that the incidence of significant neonatal neurologic morbidity and mortality was significant among nonanomalous infants who had such a pH level (23.1%). However, the remaining 76.9% of infants were neurologically normal at the time of hospital discharge.
Nor did Apgar scores predict asphyxial complications when cord pH was less than 7.0. However, the combination of an Apgar score of 3 or less and cord pH below 7.0 was a sensitive predictor of serious neonatal morbidity.
Questions abound—but not answers
It was thought that electronic fetal monitoring would eliminate intrapartum stillbirth and reduce the incidence of CP—but neither goal has been achieved. Moreover, the presence of meconium, long associated with nonreassuring fetal status, was found in one study to have no association with CP.2
As for the role of infection, inflammation, and intrapartum fever, Eastman and DeLeon suggested as early as 1955 that intrapartum fever was seven times more likely in mothers of children who were later diagnosed with CP than in mothers of normal children—and intrapartum fever, infection, and neonatal fever remain prime suspects in the CP mystery.3
How does the average clinical obstetrician interpret and use these results? How does our legal system use these results?
It depends. The overwhelming majority of nonanomalous term infants do well. For the few who develop CP, there often is an accepted reason for the diagnosis.
Graham and colleagues conclude that only 14.5% of CP cases are associated with intrapartum asphyxia. The dilemma? For that 14.5%—or even the remaining 85.5%—our ability to determine the true cause of CP in any given case is unreliable. Who or what test can conclusively eliminate intrapartum asphyxia as a medically probable cause?
The answers are disheartening.
- Recognize that prematurity and infection are the leading risk factors for cerebral palsy (CP) in nonanomalous infants.
- Be cognizant of the lack of predictive value—both positive and negative—of current methodologies, such as Apgar score and pH level, in regard to CP.
- Remember that neither the introduction of electronic fetal monitoring nor the increase in the cesarean delivery rate from 5.5% in 1970 to 31.1% in 2006 has appreciably altered the rate of CP in the United States.
- Don’t discount the importance of the first 20 minutes of postnatal life. They are perhaps at least as important as the final 20 minutes of fetal life. When delivering a patient who has a risk factor for CP, do not hesitate to request the presence of a skilled neonatologist for assistance with newborn resuscitation.—JOHN T. REPKE, MD
1. Freeman RK. Medical and legal implications for necessary requirements to diagnose damaging hypoxic–ischemic encephalopathy leading to later cerebral palsy. Am J Obstet Gynecol. 2008;199:585-586.
2. Nelson KB, Grether JK. Potentially asphyxiating conditions and spastic cerebral palsy in infants of normal birth weight. Am J Obstet Gynecol. 1998;179:507-513.
3. Eastman NJ, DeLeon M. The etiology of cerebral palsy. Am J Obstet Gynecol. 1955;69:950-961.
1. Freeman RK. Medical and legal implications for necessary requirements to diagnose damaging hypoxic–ischemic encephalopathy leading to later cerebral palsy. Am J Obstet Gynecol. 2008;199:585-586.
2. Nelson KB, Grether JK. Potentially asphyxiating conditions and spastic cerebral palsy in infants of normal birth weight. Am J Obstet Gynecol. 1998;179:507-513.
3. Eastman NJ, DeLeon M. The etiology of cerebral palsy. Am J Obstet Gynecol. 1955;69:950-961.