Induced HypothermiaInduced 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 Hypoxic Ischemic Encephalopathy (HIE)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 HIEDefinition 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: 60-66.

Long, M. and Brandon, D. Induced Hypothermia for Neonates With Hypoxic-Ischemic Encephalopathy. JOGNN. 2007; Vol.36, 3: 293-298

Conditions that can lead to Conditions that can lead to HIEHIE

Umbilical cord prolapsePlacental abruptionAcute blood lossUterine rupture

Phases of HIEPhases 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 Induced Hypothermic TherapyTherapy

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: 293-298

Induced hypothermiaEligibility criteria

◦Term or near term infant Signs & symptoms of moderate

to severe HIE Low 10 minute Apgar scoreLow cord pH or postnatal blood

pH <7.0Severe metabolic acidosis (base

deficit >16)

HIE - Nutritional ConsiderationsEligibility 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 StudyDelivery

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 kgLength: 48 cmHead Circumference: 34 cm

Case StudyDOL 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/dBase deficit 8

Case StudyDOL 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 5Ordered to PO (term infant

formula) minimum of 20 mL/kg/d Can advance to 40 mL/kg/d later in

day pending readinessTPN changed to D 9.5%, 1.5 g/kg

Trophamine; allowed lipids to run out

Case Study

Second EEG showed 20-30 second seizure activity and staring episodes

Phenobarbital started

Case StudyDOL 6Infant 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 StudyDOL 9Continued to take 150+ mL/kg/d

term infant formula~100 kcal/kg/d, 2.1g pro/kg/d

Wt: 3.150 kg, Length 51 cm, HC 34.2

97% BW, gain of 7 g/d over past week and taking all po

DischargeHome with motherFollow-up with pediatrician and

high-risk infant clinic