Induced Hypothermia Nutritional considerations for infants undergoing induced hypothermia following acute perinatal hypoxic ischemia Trayce Gardner, MEd, RD, CSP, LD Presented at Fall ONN Meeting 2011 Columbus, Ohio

Hypoxic Ischemic Encephalopathy (HIE) Linked with high-risk of morbidity (adverse neurological and developmental outcomes) and mortality Principal cause for many cases of cerebral palsy

Definition of HIE Any event that leads to a decreased oxygen and blood supply to the brain can result in hypoxic ischemic encephalopathy with both clinical and laboratory findings Selway, L. D. State of Science Hypoxic Ischemic Encephalopathy and Hypothermic Intervention for Neonates. Advances in Neonatal Care. 2010; Vol. 10, No.2: Long, M. and Brandon, D. Induced Hypothermia for Neonates With Hypoxic-Ischemic Encephalopathy. JOGNN. 2007; Vol.36, 3:

Conditions that can lead to HIE Umbilical cord prolapse Placental abruption Acute blood loss Uterine rupture

Phases of HIE Initial insult Conversion to anaerobic metabolism in the neonatal brain Subsequent abnormal brain function Accumulation of sodium, calcium, and water within the cells; potassium shifts out of the cells Cell death as a result of free radical production and cell apoptosis Secondary injury Occurs 6 to15 hours following the initial event Following resuscitation of the infant, the brain attempts to regain normal function Mitochondrial function remains impaired; inflammatory response continues to promote injury  This is the time frame in which induced hypothermia is initiated to prevent reperfusion injury

Induced Hypothermic Therapy Has been employed in clinical practice in the NICU setting since the late 1990s Selective head cooling or total body cooling Deep cooling

Nutritional Implications “Optimizing nutrition is important when caring for a neonate with HIE but is complicated by compromised bowel perfusion.” “Total parenteral nutrition is initiated and electrolytes carefully monitored.” “Adequate protein intake is necessary for growth and repair…” “The unit dietitian may aid the health care provider in reviewing the patient’s laboratory values and growth trends…” Long, M. and Brandon, D. Induced Hypothermia for Neonates With Hypoxic-Ischemic Encephalopathy. JOGNN. 2007; Vol.36, 3:

Induced hypothermia Eligibility criteria ◦ Term or near term infant Signs & symptoms of moderate to severe HIE Low 10 minute Apgar score Low cord pH or postnatal blood pH <7.0 Severe metabolic acidosis (base deficit >16)

HIE - Nutritional Considerations Eligibility criteria ◦ Term or near term infant S/S Moderate to Severe HIE Low 10 minute Apgar score Low cord pH or postnatal blood pH <7.0 Severe metabolic acidosis (base deficit >16) Baby is term or near term Need for close monitoring of TPN metabolic tolerance Concern about gut perfusion Possible low fluid/Cal needs early on – followed by high nutrition, low Cal needs later in life; need for ongoing nutrition follow- up

Case Study Maternal History and Delivery 37 year old G3 P2 with history of hypertension and sleep apnea; chronic pain – on methadone. Underwent emergency C/S due to bradycardia and NRFHT (non-reassuring fetal heart-rate tracing).

Case Study Delivery Infant had no heart rate initially; received chest compressions, intubation, and PPV (positive pressure ventilation) in the delivery room. No respiratory efforts until after moved to SCN (special care nursery) Pupils dilated and nonreactive; UVC gas, pH 6.96 and base deficit of 25; UAC gas, pH 7.09 with base deficit 20 Blood glucose 119 mg/dL; Hematocrit 51% Received NS (normal saline) bolus

Case Study 38-3/7 week infant, AGA, S/P HIE, transferred to NICU, cooling protocol initiated BW: 3.25 kg Length: 48 cm Head Circumference: 34 cm

Case Study DOL 1 – NPO (Cooling) Fluids: UVC: D10% with trophamine 2.5 g/kg and 1.5 mEq calcium/kg at 8.1 mL/hr (60mL/kg/d) UAC: ¼ Sodium Acetate at 0.5 ml/hr (3.7 mL/kg) Initial neonatal EEG obtained pH 7.23, base deficit range 7-10

Case Study DOL 2 (Cooling) TPN order: 80 mL/kg/d; D10% with 3 g Trophamine/kg/d and 1.5 g lipids/kg/d. 2 mEq Na Acetate/kg. ~51 kcal /kg/d Base deficit 8

Case Study DOL 3 (Cooling) TPN order: 80 mL/kg/d; D10% with 3 g Trophamine/kg/d and 3 g lipids/kg/d. ~56 kcal /kg/d Wt: 3.100kg (95% BW) Length 48 cm, HC 34 cm pH 7.39, base deficit 1, total protein 5.2 g/dL, albumin 2.9 g/dL, total bilirubin/direct bilirubin within normal limits (WNL)

Case Study DOL 4 (Rewarming) TPN order: 80 mL/kg/d; D11% with 3 g Trophamine/kg/d and 3 g lipids/kg/d. ~71 kcal /kg/d

Case Study DOL 5 Ordered to PO (term infant formula) minimum of 20 mL/kg/d Can advance to 40 mL/kg/d later in day pending readiness TPN changed to D 9.5%, 1.5 g/kg Trophamine; allowed lipids to run out

Case Study Second EEG showed second seizure activity and staring episodes Phenobarbital started

Case Study DOL 6 Infant continued on term infant formula; allowed to ad lib with minimum of 120 mL/kg/d Took volumes of 30 – 58 mL per feeding during the day, then 37 – 60 mL later in evening Met minimums and took closer to 152 mL/kg/d Started multivitamin at 1 mL/d for 400 IU of vitamin D due to <500 mL of formula per day and initiation of Phenobarbital

Case Study DOL 9 Continued to take 150+ mL/kg/d term infant formula ~100 kcal/kg/d, 2.1g pro/kg/d Wt: kg, Length 51 cm, HC % BW, gain of 7 g/d over past week and taking all po

Discharge Home with mother Follow-up with pediatrician and high-risk infant clinic