HIEHypoxic Ischemic Encephalopathy

Providing effective support

What we will learn

• Brief pathophysiology of HIE

• Management

• Lived experience of Families

• Strategies and supports

𝓟𝓲𝓷𝓽𝓮𝓻𝓮𝓼𝓽: ♡𝓫𝓻𝓲𝓽𝔁𝓻𝓪𝓶𝓲𝓻𝓮𝔃♡

What is HIE

• Interruption of oxygen (hypoxia) and or blood flow to the brain

• peripartum asphyxia (decreased oxygen)

• 1 per 1000 births (Levene 1986) to 6/1000 births

• problem worldwide as 10% to 60% of infants pass away

• 25% of survivors have long-term neurodevelopmental findings (Vannucci 1990).

• Treatment shown to decrease brain injury hypothermia or cooling

Brain Injury• Neuronal death occurs in two phases following

global insult (Gluckman 1992; Lorek 1994; Penrice 1996).

• immediate 'primary neuronal death' related to cellular hypoxia (primary energy failure).

• After a latent period of at least six hours, the secondary phase of delayed neuronal death' begins (Williams 1991).

Maternal Factors

• Compression of placenta

• Tearing of Placenta from uterine wall

• Compression of the umbilical Cord

• Factors effecting blood flow to baby

• Meconium Aspiration

HIE can be approached by considering the three principal clinical settings: the preterm ventilated infant, the term infant following birth asphyxia, and the infant following intrauterine compromise.

Factors that might initiate HIE are intrauterine or perinatal infection, metabolic disease, edema, hemorrhage, hypotensive events, and emboli.

Brain depends on glucose supplied by cerebral bloodflow

Neuronal death occurs in two phases following global insult (Gluckman 1992; Lorek 1994; Penrice 1996).

immediate 'primary neuronal death' related to cellular hypoxia (primary energy failure). decreased perfusion/hypoglycemia leading to metabolic acidosis, ischemia, neuronal cell death

latent period of at least six hours, secondary phase of delayed neuronal death (Williams 1991).

mechanisms involved in delayed neuronal death include edema, mitochondrialfailure, active cell death (developmental apoptosis), delayed phase is associated with encephalopathy

and increased seizure activity, and accounts for a significant proportion of the final cell loss even after very severe insults This latent phase is the therapeutic window for neuroprotective interventions

Neuronal death occurs in two phases following global insult (Gluckman 1992; Lorek 1994; Penrice 1996).

immediate 'primary neuronal death' related to cellular hypoxia (primary energy failure). decreased perfusion/hypoglycemia leading to metabolic acidosis, ischemia, neuronal cell death

latent period of at least six hours, secondary phase of delayed neuronal death (Williams 1991).

mechanisms involved in delayed neuronal death include edema, mitochondrialfailure, active cell death (developmental apoptosis), delayed phase is associated with encephalopathy

and increased seizure activity, and accounts for a significant proportion of the final cell loss even after very severe insults This latent phase is the therapeutic window for neuroprotective interventions

There is a window in which cooling will be helpful

Timing is crucial. Therapeutic hypothermia is effective in acute perinatal insults term and late preterm infants

≤6 hours old and who meet either treatment criteria Cord blood pH ≤7.0 History of acute perinatal event Apgar score ≤5 at 10 minutes or at least 10 minutes of positive-pressure ventilation (Lemyre 2018)

Cooling or Hypothermia

maintaining core body temperature between 33 degrees C and 34 degrees C For 72 hours, followed by a period of rewarming of 6 to 12 hours, is optimal.If seizures are present, antiepileptic drugs administered

Concerns are two fold

Brain Impairment• We have differing regions of brain injury

requiring life sustaining care

• Decision making by the medical team and family

• Severity of injury requiring moving from birth hospital

• Ventilation, multiple IV, feeding tubes and critical care

Stress/Pain/ Development• Separation from the family

• Unanticipated loss and grief

• Atypical sensory and motor experiences

• Possibility of inability to breastfeed

"2 days from the due date, Chandrakala and I were excited about meeting our child. We went to the hospital for a checkup just to be reassured. Nothing could have prepared us to hear doctors say that they have to do a C-section now, the baby is in distress. Our baby was born that day, and we have not held him even once because he is fighting to stay alive."

Building Capacity• Based on the premise that family

closeness provides basis for healing

• Search for strategies to understand loss and support family through grieving

• Find the space where families are connecting to their baby with one movement, one vocalization, one gesture at a time support strength and capacities

Grunau and colleagues

Greater neonatal pain-related stress was associated with poorer

quality of focused attention at 8 months CA

maternal behavior can buffer this relationship if mothers report

lower parenting stress.

This signals to me that providing buffers to stress through our

caeful determination of care is the most important part of the work.

Becoming a parent to a child with Birth asphyxia HERINGHAUS, A et al, 2013

• thrown into chaos;

• being in a state of unreality;

• being in a state of uncertainty;

• becoming a parent to a seriously ill child in a high-tech NICU environment;

• living with the experience after discharge

• the overall theme overriding an emotional rollercoaster.

Parent Experience of Neonatal Encephalopathy: The need for family-centered outcomes Lemmon, P et al ,J Child Neurol. 2017 March ; 32(3): 286–292.

“Infant outcomes are tied to family outcomes. As we work towards family-

centered outcomes in neonatal encephalopathy and other neonatal neurologic

conditions, primary data from parents can help us begin the daunting task of

defining, measuring, and improving outcomes that matter to families”

Ambiguous Loss

Difficult to explain to family and friendsThere are no rituals or finalities

Structured Interviews with families experiencing a diagnosis of HIE

• Theme 1: Many families described cumulative loss and grief throughout the perinatal crisis, critical neonatal course, and subsequent missed developmental milestones.• Theme 2: Families experienced entangled infant and broader family interests. • Theme 3: Parents evolved into and found meaning intheir role as an advocate

Children with hypoxic-ischemic encephalopathy (HIE) can have acute clinical problems, such as seizures, respiratory distress, or rapid deterioriation of consciousness. However, clinical presentation is commonly delayed. Neurological deficits might only become obvious months or years following the event.Clinical assessment of the extent or severity of the acute event is of limited prognostic value in infants. The immature brain, although more vulnerable to certain adverse stimuli, has an astonishing potential for compensatory functional development.1 Neurological deficits become more obvious when motor, cognitive, and associative demands rise above the level of basic infant functions. Walking, talking, school performance, or refined tests can reveal the limits of the brain's compensatory capacity.2

Thank youThoughts?Always open for conversationKathi FrankelKathifrankel@comcast.net