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Therapeutic Hypothermia: Treatment for Hypoxic-Ischemic Encephalopathy in the NICU

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Therapeutic Hypothermia: Treatment for Hypoxic-Ischemic Encephalopathy in the NICU Therapeutic Hypothermia: Treatment for Hypoxic-Ischemic Encephalopathy in the NICU Denise M. Casey, RN, MS, CCRN, CPNP Nancy Tella, RN, BSN, CCRN Rachel Turesky, RN, BSN Michelle Labrecque, RN, MSN, CCRN CASE STUDY admission, arterial access was established for hemodynamic Baby M was born limp, blue, and without respiratory effort at monitoring and ease of lab drawing purposes. Additional anti- 38 weeks gestation to a 38-year-old, gravida 5, para 1, woman. convulsants were given to control her seizures. Baby M’s father Delivery was vaginal after a rapid progression of labor leaving had spent the night going back and forth between our NICU no opportunity for a cesarean section. No other complications and the birth hospital because both his wife and newborn were noted during labor but a large surge at delivery, later diag- infant were quite sick. When he came in later that morning nosed as uterine rupture, initially raised concerns about placen- with Baby M’s adult stepsiblings, explanations were given for tal abruption. Apgar scores were 1, 2, and 4 at one, five, and ten each of the machines, her course of treatment up to that point, minutes, respectively. She was resuscitated in the delivery room, and our concerns about her neurologic status. Baby M’s father intubated, and transferred in critical condition to the neonatal tried to console his children despite his own fears and sadness. intensive care unit (NICU) at the birth hospital. Her initial During the next several days, Baby M remained intubated cord pH was 6.7 and was slightly improved at 7.17 on arterial for airway protection, was fluid restricted to prevent addi- blood gas after resuscitation. Our NICU team was consulted tional injury to her brain, and continued on anticonvulsants. because of her severe neurologic depression. The birth hospital Despite her traumatic delivery, Baby M remained stable from was within walking distance of our tertiary care center and our a cardiovascular standpoint without evidence of persistent neurologists went to evaluate her for the hypothermia protocol. pulmonary hypertension of the newborn (PPHN) or need Her neurologic exam was notable for dilated and unresponsive for pressors. Her kidneys were affected by the hypoxic events pupils, no spontaneous movements, and diminished reflexes at birth as evidenced by poor urine output and electrolyte and tone, consistent with moderate-to-severe encephalopathy. disturbances requiring further fluid restriction and electro- Seizure activity began at one hour of age and consisted of lip lyte boluses. Her liver enzymes were mildly elevated, but she smacking, which was later confirmed by electroencephalogram showed no evidence of coagulopathy. She was hemodynami- (EEG). Enrollment criteria were met based on respiratory cally stable after an airway was established. depression at birth requiring intubation and continued need She completed the hypothermia protocol after 72 hours for ventilation, concern for placental abruption, cord pH less of cooling and began the rewarming process. EEG tracings than 7, and encephalopathy on exam and EEG. After stabiliz- obtained on day of life (DOL) 5 showed no evidence of seizure ing her airway and achieving central access to treat acidosis and activity. Fosphenytoin was discontinued and she remained on seizures, the team prepared her for transfer to our NICU. At phenobarbital alone. A magnetic resonance imaging (MRI) this point, the primary concern became her neurologic status. of the brain done on the same day showed minor changes in Baby M was admitted to our NICU for whole-body hypo- the occipital cortex, but no significant abnormalities. thermia at four hours of age with a diagnosis of hypoxic-ischemic encephalopathy (HIE). Therapeutic hypothermia using whole- Disclosure body cooling was initiated within six hours of birth per pro- The author discloses no relevant financial interest or affiliations with any tocol with the Cincinnati Subzero Blanketrol II. Shortly after commercial interests. Accepted for publication February 2011. N EONATAL NETWORK 370 © 2011 Springer Publishing Company NOVEMBER/DECEMBER 2011, VOL. 30, NO. 6 http://dx.doi.org/10.1891/0730–0832.30.6.370 Copyright © Springer Publishing Company, LLC As she recovered and her sedation was lightened, she a biphasic process. The initial phase of hypoxic-ischemia results began to breathe and was extubated to room air on DOL 6. in a primary brain energy failure in which there are reductions Intravenous fluids were liberalized and nasogastric feedings in cerebral blood flow, oxygen, high- energy phosphorylated were initiated on DOL 7. Her neurologic exam continued to metabolites, and brain acidosis.5,6 This phase is associated with stabilize. Her pupils became reactive, suck and gag reflexes intracellular derangements such as loss of membrane homeosta- were present, and she began to move spontaneously. sis, defective osmoregulation, and inhibition of protein synthesis. She was transferred back to her birth hospital on DOL 8 to Loss of membrane homeostasis can lead to increases in intracel- continue to recuperate with her mother. At that point, she was lular calcium and osmotic dysregulation.7 Elevated calcium levels tolerating full nasogastric feedings and was consistently inter- then trigger many destructive pathways.8 Approximately 6–12 acting with her family. Additional MRI was obtained on DOL hours after the initial insult, a secondary energy failure occurs 12 and the subtle abnormalities seen earlier were no longer leading to sustained brain injury. This phase typically is without apparent. An EEG done the same day showed no evidence of brain acidosis. Secondary energy failure is a marker of the begin- seizure activity. She was discharged to home with her parents ning of multiple pathways that lead to brain injury. The processes on DOL 15 on full oral feedings and off phenobarbital. She that take place within this phase are inflammation, apoptosis, was followed in the neurology clinic every three to six months oxidative injury, decrease growth factors, and protein synthesis. for the first 24 months of life. At the last scheduled visit, Baby Because the cerebral energy state can be restored after the primary M appeared to be growing well and meeting her developmen- energy failure, it suggests there is a therapeutic window to imple- tal milestones with no apparent neurologic deficits. ment interventions to avoid or diminish the secondary energy failure leading to brain injury.6 During this biphasic process, the INTRODUCTION therapeutic window to implement interventions to reduce brain Hypoxic-ischemic encephalopathy (HIE) is defined as an injury is during the 6–12 hour window prior to the secondary interruption in the supply of oxygen (hypoxia) and/or blood energy failure. A temperature reduction of 2°–4°C decreases the flow (ischemia) going to the brain and body. This kind of rate of cell death and delays the cascade of metabolic changes interruption occurring either hours before birth or during that occur with hypoxia. Cerebral metabolism is reduced and labor and delivery can happen for several reasons such as com- hypothermia can delay secondary brain injury in HIE infants.9 pression of placenta, tearing of placenta from uterine wall, or compression of the cord. REVIEW OF EVIDENCE HIE occurs in 1/1,000 term live births and remains an In 2005, two large clinical trials of 473 infants demon- important cause of mortality and neurodevelopmental deficits strated that therapeutic hypothermia reduced the risk of in infants.1 Moderate encephalopathy carries a 10 percent risk death/disability in neonates with HIE.1,2 The major differ- of death and 30 percent risk of disability, whereas 60 percent ence between these two trials was whole-body cooling versus of those patients with severe encephalopathy die and many, if head cooling only. The Shankaran and associates trial looked not all who survive, have neurologic deficits.2 The Sarnat and at whole-body cooling with core temperature of 33.5°C by Sarnat system for neonatal encephalopathy guides the classifi- esophageal probe for 72 hours followed by a rewarming phase. cation based on Stages 1 (mild), 2 (moderate), and 3 (severe).3 There were 239 infants enrolled in this study and the inclusion The stages are classified based on the distinguishing features criteria were infants $36 weeks, admitted less than six hours shown in Table 1. Until 2005, there was no other treatment after birth, severe acidosis or perinatal complications, resuscita- for HIE other than conventional intensive care. tion at birth, and moderate-to-severe encephalopathy (clinical HIE results from a lack of oxygen and blood supply that exam only). The neurodevelopmental outcomes were assessed leads to metabolic acidosis, ischemia, and subsequently neuro- at 18–22 months of age and showed a reduced risk of death/ logic dysfunction.4 Brain injury that ensues is characterized by disability in infants with moderate-to-severe encephalopathy.2 The Gluckman and associates trial was a head cooling TABLE 1 n Sarnat Staging of Encephalopathy study and core temperature was 34°–35°C by rectal probe for Sarnat Stage 1 Sarnat Stage 2 Sarnat Stage 3 72 hours followed by a rewarming phase. The sample size was (Mild) (Moderate) (Severe) 235 term infants. The inclusion criteria for this study were term Hyperalert Lethargic Stuporous infants with moderate-to-severe encephalopathy determined Normal tone Mild hypotonia Flaccid by clinical exam and an abnormal amplitude-integrated elec- troencephalogram (aEEG). The outcomes revealed that head Overactive stretch Overactive stretch Decreased or absent reflexes reflexes stretch reflexes cooling was not protective in a mixed population of infants Weak suck Weak or absent suck Absent suck with neonatal encephalopathy. The study did show there was improved survival without severe neurodevelopmental dis- No seizures Common; focal or Uncommon 1 multifocal ability in infants with less severe aEEG changes. An article published in 2009 by Azzopardi looked at neu- Less than 24 hours 2–14 days Hours to weeks rodevelopmental outcomes in infants at least 36 weeks of age N EONATAL NETWORK VOL.
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