Tag birthinjury

In this blog, I’ll be reviewing the importance of considering genetic and metabolic disorders when evaluating neonatal encephalopathy or cerebral palsy cases.  I’ll review the features of genetic disorders that mimic encephalopathy, as well as offer recommendations specific to elements of the medical record to review when reviewing a case for merit.  Lastly, I’ll review findings in the newborn assessment that prompts suspicion for genetic causation.

Genetic conditions and metabolic disorders can mimic the signs and symptoms of neonatal encephalopathy.  In a genetically susceptible fetus (a fetus already affected by a genetic disorder), maternal infection (E.g., chorioamnionitis: an acute inflammation of the membranes and chorion of the placenta, typically due to a bacterial infection in the setting of ruptured membranes) and fetal hypoxia (inadequate oxygen supply) can compound the adverse outcomes for these newborns. 

Neonatal Encephalopathy and Hypoxic Ischemic Encephalopathy (HIE):  The recommendation is that these two terms not be used interchangeably as not all cases of neonatal encephalopathy are caused by hypoxia and ischemia (decreased blood flow).  Very few cases of cerebral palsy are due to severe hypoxia or ischemia at birth (CDC; MacLennan et al., 2015).   

• Neonatal encephalopathy is defined as a syndrome of disturbed neurological function in the earliest days of life in the infant born at or after 35 weeks of gestation manifested by subnormal level of consciousness or seizures, often accompanied by difficulty initiating and maintaining respiration and depression of tone and reflexes (AAP, ACOG, 2019).
• Neonatal encephalopathy is often mis-labeled as hypoxic ischemic encephalopathy (HIE) based on historical assumptions that all cases of neonatal encephalopathy are caused by HIE, therefore, termed HIE. This has resulted in the terms being used interchangeably (AAP, ACOG, 2019).

The Role of Genetics: Genetic susceptibility, along with the number, duration, severity and timing of insult (if applicable); gestational age; presence of fetal growth restriction; and placental function all affect cellular health and neonatal long-term outcome (AAP, ACOG, 2019).  There are multifactorial causes of neonatal encephalopathy.  Genetic causes of encephalopathy and cerebral palsy need to be considered when establishing causation.  Genetic variations are risk factors for cerebral palsy.  Examples include, but are not limited to, single nucleotide polymorphisms in genes involved in inflammation and coagulation.  Another example includes the allele of the apolipoprotein E gene associated with ischemic stroke (AAP, ACOG, 2019). The presence of variants of uncertain significance (VUS) in gene testing requires further evaluation which may include tracing the variant in other family members who have or do not have the same health condition. Variants can be either pathologic, benign, or unknown. These unknown variants involve variations in a genetic sequencing for which the association with disease risk is unclear. Therefore, the disease cannot be ruled out (NIH, 2023).

Distinguishing Neonatal Encephalopathy from Features of Genetic Disorders Mimicking Encephalopathy: Clear documentation of appropriate care and evaluation should support evidence-based conclusions. 

• Review the parents past medical history, as well as history since the birth of the affected child.
• Review the prenatal record including all fetal surveillance (non-stress tests ‘NST’s’ and biophysical profile’s ‘BPP’s’) and all ultrasounds (imaging and reports).
• Review the labor and delivery record, including the placenta pathology report and consider consultation with a placental pathologist.  Be aware of the findings associated with an increased risk of encephalopathy (E.g., funisitis ‘inflammation of the umbilical cord’ combined with a diagnostic finding of chorioamnionitis; vasculopathy ‘lesions on the placenta which can be on the fetal or maternal side causing impaired blood flow’ (AAP, ACOG, 2019).
• Review the physical examination findings of the newborn (review the newborn admission record and subsequent treating records if transfer to a higher level of care occurred).
• Review the child’s medical history for physical changes observed over time (review the following records:  pediatric, behavioral pediatric, neurology, neuropsychology, and all brain imaging performed ‘imaging and reports’).

Consider Further Evaluation: When obvious congenital defects are present at the time of birth, this should prompt further evaluation and consideration that a genetic cause may exist.  Additional diagnoses should be considered in the neonate presenting initially with encephalopathy (AAP, ACOG, 2019).

Phenotype: AAP, ACOG (2019) identifies phenotype as the observable characteristics in an individual resulting from their genes; the clinical presentation of an individual with a particular genetic constitution.

Clues in the Newborn Assessment that May Point to a Genetic Cause:

• Findings that are significant that should increase the level of suspicion that a genetic disorder may be the cause, in the presence of hypotonia, impaired level of consciousness, seizures, or periods of apnea occurring without explanation:  
  •  Disproportionate fetal growth: A small or large head circumference compared to the length of the body may point to a genetic neurological disorder. 
  • The absence of an intrapartum event (examples include, but are not limited to, a non-reassuring fetal heart rate, prolonged second stage labor, Apgar score of less than 5 at 5 minutes, placenta abruption) (AAP, ACOG, 2019)

Metabolic Disorders and Encephalopathy: Metabolic disorders (inborn errors of metabolism) may manifest in the first few days to weeks of life with features that mimic neonatal encephalopathy.  Metabolic disorders may cause or contribute to some cases of neonatal encephalopathy.  There are well over 48 known metabolic disorders that can cause neonatal encephalopathy.  Prompt identification of newborns with a metabolic disorder is essential to initiate prompt dietary changes and treatment in an effort to prevent neonatal morbidity and mortality (AAP, ACOG, 2019).

• Newborn screening is a public health service done in each U.S. state.
• Each state’s public health department decides both the number and types of conditions on its testing panel.
• Most states allow parents to opt out for religious or other reasons.
• Be aware of your state’s newborn screening program requirements.
• Every newborn should have a newborn metabolic screening performed between 24-36 hours of life.
• According to the most current CDC data available, approximately 12,500 newborns annually are diagnosed with one of the conditions detected through newborn screening. This means that almost 1 out of every 300 newborns screened is diagnosed with a metabolic disorder (NICHD).

Conclusion: When evaluating a neonatal encephalopathy and/or cerebral palsy case for causation (either medically or legally), consider the contribution of genetic and metabolic disorders.  Be aware that hypoxic ischemic encephalopathy (HIE) may mimic encephalopathy and other features associated with a genetic disorder.

Accurate diagnosis is essential, not only to establish causation, but to support the family with a plan of care with the inclusion of genetic counseling if applicable.  Accurate diagnosis is also crucial for the understanding of future risk of recurrence.

References:

American Academy of Pediatrics, American College of Obstetricians and Gynecologists, (2019). Neonatal encephalopathy and neurologic outcomes, 2^nd Ed.

Centers for Disease Control and Prevention. Retrieved on 1/26/23 from,  https://www.cdc.gov/ncbddd/cp/causes.html

MacLennan et al., 2015. American Journal of Obstetrics and Gynecology. Cerebral palsy: causes, pathways, and the role of genetic variants.

National Institute of Child Health and Human Development. Retrieved on 1/26/23 from, https://www.nichd.nih.gov/health/topics/newborn/conditioninfo/infants-screened#

National Institute of Health (2023). National Human Genome Research Institute. Variant of uncertain significance (VUS). Retrieved on 1/26/23 from, https://www.genome.gov/genetics-glossary/Variant-of-Uncertain-Significance-VUS

P.S. COMMENT AND SHARE – Do you have a complex neonatal encephalopathy or cerebral palsy case that involved multiple factors, including genetics, that influenced causation?

Barber Medical Legal Nurse Consulting, LLC is available to review complex neonatal encephalopathy and cerebral palsy cases. Email their medical legal consulting team today at: Contact@Barbermedicallegalnurse.com

In this post, I’ll be addressing the most current evidence, published standards of care, and guidelines from professional associations, and regulatory agencies specific to fetal heart rate interpretation and management. 

Fetal heart rate pattern interpretation, communication, and documentation continues to be one of the most common areas of perinatal liability claims. It is best practice to utilize current practice guidelines, and standards of care as a guide for the revisions, and development of institutional policies as a means to decrease professional liability exposure, and minimize the risk of perinatal injury.

Common Themes: In review of birth injury cases, I have observed common themes (allegations):

• Failure to interpret a non-reassuring fetal heart rate (FHR) tracing
• Failure to accurately assess maternal-fetal status
• Failure to recognize a deteriorating fetal condition
• Failure to appropriately treat an indeterminate or abnormal FHR in a timely manner (E.g., failure to initiate intrauterine resuscitation based on FHR pattern and/or plan for expeditious birth when clinically indicated)
• Failure to accurately communicate the maternal-fetal status to the physician/certified nurse midwife
• Failure to request bedside evaluation based on concern for fetal status to the physician/certified nurse midwife
• Failure of the physician/certified nurse midwife to respond appropriately when notified of indeterminate or abnormal fetal status
• Failure to initiate the chain of command (communication) when there is a clinical disagreement between the nurse, and responsible physician/certified nurse midwife, regarding fetal status   

Standards of Care:

• Use of EFM definitions and descriptions based on the 2008 National Institute of Child Health and Human Development (NICHD) Working Group findings (ACOG Practice Bulletin, Intrapartum Fetal Heart Rate Monitoring, 2017)
• In the presence of an EFM tracing with minimal or absent variability, and without spontaneous accelerations, an effort should be made to elicit accelerations by means of vibroacoustic stimulation, or scalp stimulation.  When there is an acceleration with stimulation, acidemia is unlikely, and labor can continue (ACOG Practice Bulletin, Intrapartum Fetal Heart Rate Monitoring, 2017).
• Be aware of the EFM findings consistent with an abnormal acid-base status: absence of accelerations; minimal to no variability (ACOG Practice Bulletin, Intrapartum Fetal Heart Rate Monitoring, 2017).
• Be aware of when to implement intrauterine resuscitation based on interpretation of EFM: Category 2, and category 3 FHR tracings, uterine tachysystole (dependent on FHR pattern, and presence or absence of oxytocin (ACOG Practice Bulletin, Intrapartum Fetal Heart Rate Monitoring, 2017).
• Implement intrauterine resuscitation based on the presumed etiology of the FHR pattern: maternal repositioning, intravenous fluid bolus, oxygen administration (if oxygen is being administered for intrauterine resuscitation, oxytocin should be discontinued), reduction of uterine activity, correction of maternal hypotension, amnioinfusion, modification of maternal pushing efforts during second stage labor (AWHONN Perinatal Nursing, 2021).
• Be able to recognize uterine tachysystole: 5 contractions in 10 minutes, averaged over 30 minutes. 
• Be aware of the interventions to manage tachysystole in the presence, and absence of oxytocin.  E.g., uterine tachysystole in the presence of oxytocin with a Category 1 tracing requires a reduction in oxytocin.  Uterine tachysystole in the presence of oxytocin with a Category 2 or 3 tracing requires a reduction or discontinuation of oxytocin, and implementation of intrauterine resuscitative measures.  If no resolution, a tocolytic should be considered.
• During induction or augmentation of labor with oxytocin, the FHR should be evaluated and documented before each dose increase, and following each dose increase (AWHONN Position Statement, Fetal Heart Monitoring, 2015)
• If continuous EFM is ordered, monitoring of FHR, and uterine activity should continue until birth (AWHONN Perinatal Nursing, 2021).
• Development of institutional policies, procedures, and protocols that outline responsibility for ongoing FHM documentation (AWHONN Position Statement, Fetal Heart Monitoring, 2015).
• Documentation should include communication with providers (AWHONN Position Statement, Fetal Heart Monitoring, 2015).
• Documentation should include communication within the chain of resolution / chain of command (AWHONN Position Statement, Fetal Heart Monitoring, 2015).
• Ongoing education and competency validation for RN’s, and other healthcare providers responsible for FHM (AWHONN Position Statement, Fetal Heart Monitoring, 2015).
• Use of oxytocin safety checklists are recommended as they provide prerequisites to safely initiate oxytocin, and to help identify situations that require discontinuation (ACOG Optimizing Protocols in Obstetrics, Oxytocin for Induction, 2011).  

References:

ACOG (2011). Optimizing protocols in obstetrics, Oxytocin for induction   

ACOG (2017). Practice Bulletin, Intrapartum fetal heart rate monitoring

AWHONN (2021). Perinatal nursing

JOGNN (2015). AWHONN position statement: fetal heart monitoring

P.S. Comment and share your experience with a birth injury case related to fetal monitoring interpretation, communication and/or documentation.

In this blog I’ll be reviewing the difference between rotational and non-rotational maneuvers in the management of a shoulder dystocia.  I’ll also discuss the efficacy in relieving the shoulder dystocia, and the risk of brachial plexus injury, comparing both types of maneuvers.   

Non-rotational maneuvers: pose the least risk on the degree of stretch on the brachial plexus nerve.  Examples include: McRoberts maneuver, suprapubic pressure, and delivery of the poster arm. 

According to ACOG, in cases where the McRoberts maneuver and suprapubic pressure are unsuccessful, delivery of the posterior arm can be considered as the next maneuver to manage shoulder dystocia. Recent evidence has shown that delivery of the posterior arm has a high degree of success in accomplishing delivery.  In a computer-generated model, delivery of the posterior arm required the least amount of force to effect delivery and resulted in the lowest amount of brachial plexus stretch.  The use of the above maneuvers will relieve 95% of cases of shoulder dystocia within 4 minutes. 

Below Image (delivery of the posterior arm) requires the delivering provider to insert a hand into the vagina and deliver the posterior arm by sweeping it across the fetal chest

Rotational maneuvers: Examples include: The Rubin maneuver,  the Woods Screw maneuver

• The Rubin maneuver requires the delivering provider to insert a hand into the vagina and on the back surface of the posterior fetal shoulder.  The provider then rotates the fetal shoulder anteriorly towards the fetal face with his/her hand.
• The Woods Screw maneuver requires the delivering provider to rotate the fetus by exerting pressure on the anterior, collar bone region of the posterior shoulder to turn the fetus until the anterior shoulder emerges from behind the maternal symphysis (pubic bone).

Below Image (Rubin Maneuver)

References:

The American College of Obstetricians and Gynecologists. (2014). Neonatal brachial plexus palsy. ACOG Task Force on Brachial Plexus Palsy

The American College of Obstetricians and Gynecologists. (2017). Shoulder dystocia [Clinical Practice Bulletin #178]

 P.S. Comment and Share: What has been your experience in a brachial plexus case involving a shoulder dystocia?  How did the standards of care, specific to type of maneuvers, and type of traction employed, impact the outcome of the case?  

All adverse outcomes cannot be prevented; however, defensibility is strengthened when care rendered is consistent with standards of care.

In this blog I’ll provide a brief overview of Hypoxic Ischemic Encephalopathy (HIE) neonatal brain injury.  I will review the definition, the incidence (U.S. and worldwide), associated complications, possible causes, and recommended treatment.  I will also share possible defenses to consider when developing a HIE neonatal brain injury case. 

What Is It? HIE neonatal brain injury is injury to the brain as a result of hypoxia.  Hypoxia is a deficiency of well oxygenated tissue.  This can result from a combination of insufficient blood flow and/or decreased oxygen levels. 

How Common Is HIE? HIE is the leading cause of brain injury in the perinatal period.

• Occurs in 1 to 8 of every 1,000 live births in the United States
• HIE causes 30% of cerebral palsy cases in the United States
• HIE causes 23% of neonatal deaths world-wide. The fifth leading cause of deaths worldwide in children under 5 years of age (World Health Organization, 2020).

Complications of HIE (including, but not limited to…): cerebral palsy, epilepsy, mental retardation, visual impairment, hearing impairment, learning disabilities, cardiac arrest, death.

Causes (including, but not limited to…) of HIE neonatal brain Injury: (literature suggests 70-80% of HIE neonatal brain injury cases are not preventable)

1. Antepartum and Intrapartum Events – placental abruption, umbilical cord prolapse, uterine rupture, acute blood loss (maternal hemorrhage), infection
2. Maternal Underlying Risk Factors – hypotension, hypertension, placental vasculopathies, insulin dependent diabetes
3. Neonatal Risk Factors – congenital heart disease, pulmonary disease, severe apnea, patent ductus arteriosus, hypoglycemia, hyperglycemia, meconium aspiration syndrome, infection

Treatment:  Therapeutic hypothermia, or induced cooling, has been shown to reduce death and disability in many HIE cases.  Reduction in the core body temperature reduces the brain temperature resulting in neuroprotection.  Therapeutic hypothermia is the standard of care for infants who are diagnosed with moderate to severe HIE following birth (no later than 6 hours of life) and who meet specific criteria per standard of care adopted by organizational policy, procedure, and order set. 

*Sarnat Staging System is the standard of care to grade severity of HIE

Cooling can be done on the whole body, or through a cooling cap placed on the head.  The infant may need other medical interventions to support their organs or to treat seizures.

Infants who experience HIE may require early intervention therapy services after discharge.  These include services from a neurodevelopmental pediatrician, physical therapist, occupational therapist, speech therapist, feeding and swallowing therapist, and/or a pediatric neurodevelopmental ophthalmologist.

Possible Plaintiff Allegations for HIE Neonatal Brain Injury:

Failure to transfer mother to tertiary care center (higher level of care)

Failure to or delay in transferring infant to Level III NICU for hypothermia therapy

Failure to attend or delay in arrival of a NICU team to a high-risk delivery

Failure of medical staff to recognize and treat neonatal seizures

Failure of Midwife to have appropriate resuscitative equipment and personnel for home delivery

Failure to follow hypothermia treatment protocol

Possible Defenses for HIE Neonatal Brain Injury:

The infant did not meet criteria for hypothermia protocol

The manifestations of the brain injury were metabolic or genetic in nature and not a result of HIE

The infant was not stable for transport to a higher level of care

The mother was non-compliant with regimen for high-risk pregnancy conditions

The mother had no prenatal care

Synthesis of Data and Case Development:  Knowing which relevant maternal and infant medical records to request and what questions to ask are essential.  Having an awareness of standard physician orders, and standing nursing orders will support the development of a case.  A strong understanding of the electronic medical record and documentation requirements, as well as standard laboratory and diagnostics ordered will support case development. 

Below are some clinical areas of focus for case development:

• pathophysiology of fetal monitoring and fetal strip interpretation: identification of fetal hypoxia
• acid-base balance: identification of fetal and/or neonatal metabolic acidosis
• newborn Apgar scoring: identification of the presence of birth asphyxia
• gestational age assessment: evaluation of the appropriateness of implementing hypothermia treatment
• staging and classification criteria for HIE: identification of the level of neurological compromise, identification of eligibility criteria of newborn for hypothermia treatment
• hypothermia treatment: identification of treatment as the standard of care, criteria for treatment, treatment modalities, procedure, staff competencies and continuing education

Perinatal Safety and Professional Liability: All adverse outcomes cannot be prevented; however, defensibility is strengthened when care is consistent with relevant, current evidence-based practice recommendations and standards of care. 

P.S. Comment and Share: What were your successes and challenges working through a HIE birth injury case?

References:

Douglas-Escobar & Weiss. (2015). Hypoxic-Ischemic Encephalopathy: A review for the clinician. JAMA pediatrics. 169(4):397–403. doi:10.1001/jamapediatrics.2014.3269 

Simpson K.R., & Creehan P.A. (2020). AWHONN’s Perinatal Nursing. 5^th edition. Lippincott Williams & Wilkins

World Health Organization. (2020). Newborns: improving survival and wellbeing. https://www.who.int/news-room/fact-sheets/detail/newborns-reducing-mortality

World Health Organization. (2022). The top 10 causes of death. https://www.who.int/news-room/fact-sheets/detail/the-top-10-causes-of-death