1.

Definisi HIE
2. Epidemiologi HIE
3. Therapeutic hypothermia for HIE
4. Keberhasilan TH for HIE

Therapeutic hypothermia should be started after the resuscitation in newborns >36 weeks
gestation with clinical or laboratory evidence of moderate to severe HIE.

Therapeutic hypothermia is now the gold standard treatment for infants with moderate to
severe HIE, whereby the infant’s core body temperature is decreased within 6 hours after
birth followed by slow rewarming for neuroprotection. This treatment slows the metabolic
rate so cells can recover and prevent further damage. It has been shown to improve survival
and outcome and reduce the risk of death or major neurodevelopmental disability at 18
months of age with data suggesting that the long-term benefits resulted in improved
neurocognitive outcomes persisting into middle childhood. The treatment should start within
the first 6 hours after birth with systemic temperatures between 33⁰ and 35⁰ and continuing
treatment for a total of 72 hours. A 2013 Cochrane review provided evidence from 11
randomized controlled trials (n = 1505 infants) that TH is beneficial in term and late preterm
newborns with moderate to severe HIE. (bab 43, Therapeutic hypothermia, hal. 388) It
reduced mortality and neurodevelopmental disability. Thus, hypothermia therapy is the
standard of care for newborns with moderate to severe HIE. It attenuates secondary energy
failure by decreasing cerebral metabolism, inflammation, excitotoxicity, oxidative damage,
and cellular apoptosis. TH is currently not recommended for infants with mild
encephalopathy, but some studies are investigating this area as well. (bab 110, neonatal
encephalopathy, hal. 1003)

There are 2 types of cooling, selective head cooling (SHC) and whole-body cooling (WBC),
which is more common. Selective head cooling is done by using a cooling cap that circulates
cold water that is placed on the infant’s head to lower the core temperature. Whole body
cooling is done by using a cooling blanket or different types of wraps or mattresses that
circulate cold water that is placed under the baby to lower the total body temperature. (sama)

Blood pH of ≤7.0 or base deficit of ≥16 mmol/L and a complete neurologic examination
through Thompson Score which then proves a moderate to severe HIE in the infant, or if
seizure is documented or reported, infant is automatically eligible for cooling. (sama, tp hal.
388-389)

HIE has an incidence of 1.5 per 1000 live births. (bab 110, neonatal encephalopathy, hal.
998)

Periventricular leukomalacia (PVL) is necrosis and gliosis of periventricular white matter.

Although more common in preterm infants, it can be seen in term infants with HIE. (sama
dgn diatas, hal.999)

Clinical presentation includes deep stupor or coma, respiratory failure due to poor central
drive, diffuse hypotonia with minimal movement, and focal clonic seizure in term infants or
generalized tonic seizure in preterm infants. (sama)

It occurs in 1.5 to 2.5 per 1000 live births in developed countries. 40–60% of affected infants
die by 2 years of age or have severe disabilities including mental retardation, epilepsy, and
cerebral palsy (CP). HIE is a brain injury that prevents adequate blood flow to the infant’s
brain occurring as a result of a hypoxic-ischemic event during the prenatal, intrapartum or
postnatal period. HIE is a disorder in which clinical manifestations indicate brain
dysfunction. While the exact cause is not always identified, antecedents include cord
prolapse, uterine rupture, abruptio placenta, placenta previa, maternal hypotension, breech
presentation, or shoulder dystonia. The manifestations of perinatal HIE in early postnatal life
include abnormal fetal heart rate tracings, poor umbilical cord gases (pH < 7.0 or base deficit
≥ 12 mmol/L), low Apgar scores, presence of meconium stained fluid, or the need for
respiratory support within the first several minutes of postnatal life. Health care providers
also use the Sarnat staging criteria or an adapted version to describe the severity of
encephalopathy within the first several postnatal days of life in conjunction with
neuroimaging to assess the severity of the insult. (Allen K.A., Brandon D.H. Hypoxic
Ischemic Encephalopathy: Pathophysiology and Experimental Treatments. Newborn
Infant Nurs. Rev. 2011;11:125–133. doi: 10.1053/j.nainr.2011.07.004.)

Perinatal hypoxic-ischemic encephalopathy (HIE) is a childbirth complication most

commonly induced by intrauterine asphyxia. HIE is a major problem worldwide as 10% to
60% of affected infants die, and at least 25% of survivors have long‐term
neurodevelopmental sequelae. Therapeutic hypothermia is the standard treatment for neonatal
HIE, due to its proven efficacy in reducing infant mortality and brain injury by 25%, and in
reducing the risk of CP by 34%. (Jacobs SE, Berg M, Hunt R, Tarnow-Mordi WO, Inder
TE, Davis PG. Cooling for newborns with hypoxic ischaemic encephalopathy. Cochrane
Database Syst Rev. 2013 Jan 31;2013(1):CD003311. doi:
10.1002/14651858.CD003311.pub3.)

In clinical practice, neonates begin hypothermia within 6 h of birth and are typically
maintained at 33.5 ± 0.5°C for 72 h. (Shankaran S, Laptook AR, Pappas A, McDonald SA,
Das A, Tyson JE, et al. Effect of depth and duration of cooling on death or disability at
age 18 months among neonates with hypoxic-ischemic encephalopathy: a randomized
clinical trial. JAMA (2017) 318:57–67.10.1001/jama.2017.7218)