CASE STUDY NEONATAL HEAD COOLING

Running head: CASE STUDY NEONATAL HEAD COOLING 1

Case Study 1: Head Cooling as Treatment for Neonatal Encephalopathy

NURS 6035 Practicum I

Teresa Z. Baker

Texas Woman’s University

CASE STUDY NEONATAL HEAD COOLING 2

Case Study 1: Head Cooling as Treatment for Neonatal Encephalopathy

Preliminary Information

Selection of Case

Previously, I worked in a Level IV Neonatal Intensive Care Unit (NICU) which provided

head cooling therapy for the treatment of neonatal encephalopathy. Currently I am working in a

smaller NICU which is not equipped nor trained to provide this therapy. The smaller NICU,

however, transports neonates with hypoxic ischemic encephalopathy to the Level IV NICU that

does provide head cooling therapy. I selected this case because it presented the opportunity to

not only learn about head cooling therapy, but how to prepare and transport an infant who is

being transferred for head cooling therapy. There is little literature available regarding preparing

an infant for transport to a cooling center. As studies have demonstrated positive results with

cooling therapy, the treatment has become more popular. Due to the small number of cooling

centers available in Texas, there have been an increased number of infants being transported for

cooling therapy as treatment of neonatal encephalopathy. I wanted to share this information with

my peers for whom transporting an infant for cooling therapy may become necessary.

Type and Number of Encounters

M.P. was delivered in an outlying hospital and was admitted to the NICU for respiratory

distress and perinatal asphyxia. Shortly after birth, infant was transported to a larger NICU which

provided adequate testing and cooling therapy for asphyxiated infants.

Insurance

This patient is on the state-funded Medicaid plan.


Subjective

Patient Profile

M.P. is a newborn Hispanic female, who delivered at 38 3/7 weeks gestation. She was

admitted to the Neonatal Intensive Care Unit (NICU) from the delivery suite.

Background Information

CC. Patient was born with perinatal asphyxia. M.P. was admitted to the NICU for

Hypoxic-Ischemic Encephalopathy.

HPI. Infant was delivered emergently in the operating room for fetal bradycardia.

PMH.

Birth. M.P. was 38 3/7 weeks gestation, delivered by emergent caesarean section to a

gravida 1, Para 1, 20-year old Hispanic female, who received prenatal care at the Prenatal

Clinic. The pregnancy was complicated by increased glucose and was diet-controlled.

There was no exposure to medications, alcohol, recreational drugs, or tobacco. Her

prenatal screening labs were negative. Labor was complicated by meconium stained

amniotic fluid and maternal transient hypotension after an epidural was administered.

The hypotension improved with positioning and a dose of Ephedrine. Following the dose

of Ephedrine, severe fetal bradycardia was noted via scalp electrode monitoring. Mother

was transferred to the operating room and an urgent caesarean section was performed.

By the time of delivery the infant had been without a detectable heart rate for at least five

minutes.

Birth time: 2323 on 8/19.

Birth weight: 2675 grams.

Length: 49.5 centimeters.


Head circumference: 32 centimeters.

Apgars: 0 at one minute; 2 at five minutes; 3 at ten minutes.

M.P. delivered with meconium stained amniotic fluid. Tone was floppy, color was pale,

no respiratory effort or heart rate was noted at the time of birth. She was intubated with a

3.5 endotracheal tube (ETT) and meconium was suctioned from below the vocal cords.

Bulb suctioning was performed and face mask ventilation was initiated. Despite

ventilation, no heart rate was noted at one minute of age. Chest compressions were

started and the infant was reintubated with a 3.5 ETT. Bag ventilation was initiated.

No heart rate was detected for 3 minutes of chest compressions and ventilation.

Epinephrine was given through the ETT. After approximately 30 seconds, a heart rate

was detected, which gradually increased to a rate of 150 beats per minute. M.P. was pink

with improved perfusion but continued to have floppy tone, was unresponsive, and had

occasional agonal breaths. She was transferred to the NICU for further management.

M.P. was placed on the conventional ventilator. A peripheral intravenous catheter was

placed. An umbilical venous catheter was placed and an umbilical arterial catheter was

attempted without success. Blood was drawn for a complete blood count (CBC), blood

cultures, and a blood gas. The CBC showed a left shift, with 34 neutrophils and 18

bands. Ampicillin and Cefotaxime were started until sepsis could be ruled out.

Ventilator settings were adjusted based on the blood gas. Since perinatal asphyxia was

suspected from the history of events, M.P. was placed in a radiant warmer with all heat

turned off and a temperature probe in place. The temperature was targeted at 33 degrees

Celsius. D10W intravenous fluid was initiated, but restricted to 60 milliliters per

kilogram (mg/kg) per day. The initial blood glucose was 110 milligrams per deciliter.


One hour. At approximately one hour of age, M.P. was noted to have seizure activity

with eye blinking, posturing and tremulous movement of the upper and lower extremities.

The initial pH on the arterial blood gas was 6.87, paCO2 was 95 and the base excess was

-19.0, showing metabolic acidosis. A 10 milliliter bolus of Sodium Bicarbonate was

given. A repeat blood gas drawn, following the bolus and ventilator changes, showed

marked improvement. The pH increased to 7.22, the paCO2 decreased to 27 and the base

excess improved to -15. Her blood pressure was 40/26 (33) and a 10 ml/kg normal saline

bolus was given intravenously. Dopamine and Dobutamine were initiated intravenously

for hypotension and hypoperfusion. Phenobarbital was given for seizure activity. The

cooling center was contacted and the transport team was dispatched to the outlying

hospital to transport the baby.

Two hours. M.P. continued to have seizure activity and a dose of Keppra was given

intravenously. The temperature was maintained between 32 and 34 degrees Celsius.

The transport team arrived and obtained an arterial blood gas. The pH was 7.34,

paCO2 was 29, and base excess had improved to -10 from the previous blood gas. The

infant was transferred to the transport incubator, with no heat applied. Skin temperature

probe was applied.

Parents and grandparents were allowed to visit with M.P. while the transport team

were readying for departure. Their questions were answered and directions to the

destination cooling center were given. The transport team departed with the infant via

helicopter at approximately two and one half hours of age. At this time, care was

assumed by the staff of the cooling center.


Four hours. Word was received that M.P. had arrived at the cooling center. According

to report, a 20 minute amplitude-integrated electroencephalogram (aEEG) was done to

assess for seizures and neurological status. M.P. continued to have seizure activity after

arrival at the cooling center.

Five hours. M.P. was placed on the head cooling apparatus at approximately five hours

and 20 minutes of age. She remained on the head cooling therapy for 72 hours and

gradually rewarmed.

Two to twenty days. The cooling center reported that M.P. had weaned off the ventilator

to nasal cannula and off pressors on the fourth day of life (DOL). She weaned off nasal

cannula to room air on the ninth day of life. M.P. had been on hyperalimentation fluids

(HAF) that were adjusted daily to maintain laboratory results in normal range. HAF was

tapered off as nipple feeding with 22 calorie formula improved. M.P. was on a

maintenance dose of Keppra with no further evidence of seizures. A magnetic resonance

imaging (MRI) study conducted on the fifth day of life was unremarkable. The aEEG

showed diffuse slowing with no seizure activity. A 24-hour video EEG did not show

seizures.

M.P. gradually increased feeding to ad lib by nipple with 22 calorie formula,

voiding and stooling normally, and having no further seizure activity on Keppra.

M.P. roomed in with her parents and was discharged on DOL 20.

Medications. Keppra 66.9 mg, by mouth, every 12 hours.

Family History.

Mother. Hispanic female who speaks English. She does not work outside the home.


Father. Hispanic male who speaks Spanish. He is employed full time as a construction

worker. Mother reports that he is in “good health”.

Additional family information. There are no other children in the family. M.P. will be

living with her biologic mother and father. The family resides in a private home in Bryan.

They are currently receiving state funded insurance. There are no reported genetic

disorders on either side of the family.

Social History. M.P. has extended family that lives nearby. The maternal grandparents

were present at the delivery and are very supportive. The family religion is Catholic and

the family attends church regularly.

Review of Systems on Admission.

Head/Neck. Appears normocephalic. No dysmorphic features.

Skin. Warm and dry to touch. No rashes or birthmarks noted.

Eyes. Normal placement. Red reflex present bilaterally. Sluggish pupillary response.

Ears. Normal placement.

Nose. Normal placement.

Oropharynx. Infant is intubated. Feeding tube to gravity.

Cardiac. Normal sinus rhythm. Decreased perfusion. No murmur noted.

Respiratory. Breath sounds equal and clear, on conventional ventilator. Occasional

spontaneous respirations noted. Good air movement.

Abdomen. Soft, non-distended, no masses or organomegaly. Faint bowel sounds heard.

Three vessel cord, stained with meconium. Umbilical venous catheter in place.

GU. Normal term female genetalia. No stool or urine output since birth.

Neuro. Depressed since birth.


Extremities. Occasional tremulous movements noted. Seizure activity noted.

Growth/Development. Infant is appropriate for gestational age. Unable to assess

development at this time.

Objective

Physical Examination

General. M.P. is a term, female newborn, on conventional ventilator, lying quietly in

radiant warmer with the heat turned off.

Vital Signs. T: 95 Rectally. HR: 130. RR: 40 (SIMV). BP: 40/26(33)

Weight. 2.675 kg.

Length. 49.5 cm.

Head Circumference. 32 cm.

Head/Neck. Head appears normocephalic. Anterior fontanel soft, flat. No scalp edema

noted. Neck supple.

Skin. No abnormalities noted.

Eyes. Red reflex bilaterally. Sluggish pupillary reaction.

Ears. Normal placement. No discharge or tags noted.

Nose. Nares patent. Good air movement.

Orophyarynx. ETT in place. Orogastric tube in place to gravity. Palate intact. No

abnormalities noted.

Cardiac. Heart sounds normal with no murmur noted. Decreased perfusion, but

improving. Femoral pulses strong.


Respiratory. Chest is symmetric. Nipples are normally placed. Breath sounds equal,

clear, good air movement, on conventional ventilator. Vent settings: Rate 40, Peak 22,

Peep 5, Itime: 0.40. FiO2 .45.

GI. Abdomen soft, flat, no masses or organomegaly. Umbilical venous catheter in place.

Three vessel cord with meconium staining.

GU. Normal term female genetalia. Anus patent with normal wink.

Extremities. Normal appearance of upper and lower extremities. Normal creases.

Peripheral catheter in place in left foot.

Back. Spine appears straight. No sacral dimple noted.

Neuro. Hypotonia of trunk. Hypertonia of extremities. Occasional tremulous

movements of the upper and lower extremities. Brief opisthotic posturing. No suck or gag

reflex elicited. No response to painful stimuli.

Musculoskeletal. Decreased tone in trunk. Increased tone in extremities.

Growth/Development. Infant appears appropriate size for gestational age. Unable to

assess development at this time.

Diagnostic Tests.

The following test results were obtained and discussed with parents.

Complete blood count. Values normal except for left shift on the differential.

Blood cultures. Blood cultures were negative for sepsis.

Blood gases. Blood gases were initially abnormal, but were corrected with conventional

ventilation and sodium bicarbonate and normal saline boluses.

Infant was referred to a cooling center for assessment of hypoxic-ischemic

encephalopathy to include head cooling selection criteria, aEEG, video EEG, Sarnat


Score, and MRI.

Head cooling criteria: M.P. met Criteria A, B, and C for head cooling therapy.

Discussion of Findings

Hypoxic-ischemic encephalopathy (HIE) is a term used to describe the condition

resulting from reduced oxygen to the brain, before and/or during the delivery of an infant. HIE

is a serious condition that causes significant mortality and morbidity in the neonatal population.

This condition affects 1-8 neonates per 1000 births and can result in major brain injury (Zanelli,

Stanley, & Kaufman, 2009). “Preventing the secondary reperfusion injury that occurs following

a hypoxic-ischemic event is paramount to ensuring the best possible neurologic outcome for the

neonate” (Long & Brandon, 2007).

“Seizures increase the risk of neurological sequelae by as much as forty fold. Early

onset of seizures increases the risk of adverse outcome and the risk is approximately 75 percent

with onset in the first four hours” (Volpe, 2008, p 441). Seizures may cause further injury to the

brain. The long-term sequelae may include mental retardation, seizures, cerebral palsy, epilepsy,

blindness, hearing impairment, learning disability, and other mental and psychomotor deficits.

Magnetic resonance imaging (MRI) study is the most accurate diagnostic test for hypoxic

ischemic injury in the newborn (Volpe, 2008, p.414).

Recent studies have suggested that cooling therapy is of benefit for the outcome of

infants with HIE (Zanelli, Stanley, & Kaufman, 2009). The National Institute of Child Health

and Human Development Neonatal Research Network conducted a large, multicenter,

randomized trial from 2000 to 2003 and found that whole body cooling significantly reduced the

risk of death or disability for neonates diagnosed with moderate or severe HIE ( Shankaran et al.,

2005). The beneficial mechanism for hypothermia appears to be partially in relation to reduction


of energy consumption and decrease in the accumulation of extracellular glutamate (Volpe,

2008, p. 460).

There is a therapeutic window of opportunity during which hypothermic intervention can

decrease the amount of cell death resulting from secondary energy failure. If selective

brain cooling can be initiated during the first 6 hours after the injury and the baby’s brain

is kept cool for the duration of the secondary energy failure state, science has

demonstrated selective head cooling can interrupt the second phase of the injury and have

a significant effect on the severity of the secondary cell death (www.natus.com).

Asphyxiated neonates have complex medical needs and should be cared for in intensive

care units that can provide multidisciplinary subspecialty evaluation and treatment. Most

neonates who meet the criteria for hypothermia therapy will be born in hospitals that do

not provide this high level of care (Fairchild, Sokora, Scott, & Zanelli, 2010).

Since many of the neonates who deliver with perinatal asphyxia are born in remote

hospital settings, investigation into how best to manage these patients in a safe and timely

manner is warranted, to avoid long-term sequelae (Zanelli, Stanley, & Kaufman, 2009).

Neither the NICHD nor the CoolCap trial recommended cooling before arrival

at the study center (Anderson, Longhofer, Phillips, & McRay, 2007).

Clinical evidence of moderate to severe HIE is defined by criteria A, B, and C below.

The infant should meet these three criteria to be considered a candidate for head cooling therapy.

Criteria A. Infant at > 36 weeks gestational age and at least one of the following:

Apgar score <5 at 10 minutes

Continued need for resuscitation, including ventilation at 10 minutes after

birth.


Acidosis defined as arterial pH < 7.00 within 60 minutes of birth.

Base excess < -16 mmol/L within 60 minutes of birth.

Criteria B. Infant with moderate to severe encephalopathy consisting of altered state of

consciousness (as shown by lethargy, stupor, or coma) and at least one of the following:

Hypotonia

Abnormal reflexes, including oculomotor or papillary abnormalities

Absent or weak suck

Clinical seizures

Criteria C. Infant has an aEEG recording of at least 20 minutes duration that shows

either moderately severe abnormal aEEG background activity OR seizures

(www.natus.com).

Assessment

Diagnoses

Acute Diagnoses

Hypoxic-Ischemic Encephalopathy (768.5). M.P was born with perinatal asphyxia.

Asphyxia is defined by: pH on blood gas < 7.00, Apgar score of 0-3 for more than five

minutes after birth, neurologic manifestation in the immediate neonatal period (seizures,

hypotonia, coma), and evidence of multi-organ system dysfunction in the immediate

neonatal period (Zanelli, Stanley, & Kaufman, 2009).

Chronic Diagnoses

1. Seizures (779.0). HIE is often the most frequent cause of neonatal seizures. Infarcts

occur with neonatal seizures in 80% of patients. Subtle seizures may occur with HIE

(Zanelli, Stanley, & Kaufman, 2009). M.P. began having seizures within an hour


after birth which were controlled with medication. She was discharged on Keppra

for the prevention of seizures.

2. Developmental Delay (783.40). Monitoring specific developmental milestones are

essential for determining the presence of delay. These milestones include cognitive, fine

and gross motor skills (Feigelman, 2007).

Differential Diagnosis

Posterior Cerebral Fossa Hemorrhage (767.0). On occasion, difficulties with delivery,

particularly with breech presentation, hemorrhage in the posterior cerebral fossa should be

considered as an alternate diagnosis. However, this is a rare condition (Zanelli, Stanley, &

Kaufman, 2009). Posterior cerebral fossa hemorrhage usually occurs in full term infants with a

traumatic breech or forceps delivery.

Typical signs include: apathy, irritability, vomiting, high-pitched crying, respiratory

insufficiency, bradycardia, tense anterior fontanelle, increased circumference of the

head, hypotonia, nystagmus, palsies of diverse cranial nerves, depression of primitive

reflexes, coma and seizures. Diagnosis is verified by computerized topography (CT) scan

or sonography. Other important data include blood-tinged cerebral spinal fluid, a fall of

hemoglobin concentration and intraretinal hemorrhage. Electroencephalogram (EEG)

are often normal (von Gortand, Arnold, & Adis, 1988).

M.B. had no evidence of hemorrhage on MRI.

Impressions

Infants who survive severe HIE, may have persistent feeding difficulties requiring tube

feeding for weeks to months. (Zanelli, Stanley, & Kaufman, 2009). When M.P. was discharged


from the hospital at 20 days of age, she was nipple feeding well. She was gaining weight on 22-

calorie formula. It will be important to track her feedings and weight trends.

M.P. should be monitored for seizures. The MRI performed at five days of age was

unremarkable. A 24-hour video EEG did not show seizures, on a maintenance dose of Keppra.

She was discharged on Keppra at 66.9 mg, by mouth, every 12 hours. She has had no recurrence

of seizures. She should be followed by a pediatric neurologist.

It is essential that M.P. be monitored for cognitive, fine, and motor skills to determine

potential presence of developmental delay (Feigelman, 2007). Among infants who survive

moderately severe HIE, 10-20% have minor neurological morbidities. In the absence of obvious

neurological deficits in the neonatal period, there may be long-term functional impairments.

Children with a history of moderate to severe HIE should be monitored into school age (Zanelli,

Stanley, & Kaufman, 2010).

The patient has a very supportive family who is attentive to her needs. Both parents and

grandmother are very proficient at feeding M.P.

M.P. should be assessed in the future for the need for the Early Childhood Intervention

program. In the event that developmental delays or learning disabilities are assessed, this

program would benefit M.P. by providing occupational therapy, physical therapy, and a number

of other different services, at no cost.

Immediate Plan

Neurological Assessment

1. Evaluate neurological status

2. Establish need for hypothermia treatment according to criteria for hypoxia.

Transport


1. Initiate contact with cooling therapy center regarding potential preparation and

expedient transport of infant hypothermia.

Passive Cooling

1. Upon approval by accepting center, begin passive cooling until arrival of transport

team.

2. Maintain rectal temperature at 33oC to 35

oC as directed by cooling center.

Blood Pressure Management

Maintain blood pressure within normal limits with Dopamine, Dobutamine

Fluid Management

Assure fluid restriction at 60-80 ml/k/d.

Seizure Management

1. Administer medications to control seizures.

Rationale: Educating referring clinicians about when and how to initiate therapeutic

hypothermia is a cornerstone to a successful program. It is recommended that in cases of acute

perinatal distress with suspected HIE, the radiant warmer should be turned off and the baby’s

temperature closely monitored during initial stabilization and neurological assessment. If the

neurological examination is not consistent with moderate to severe encephalopathy, the baby

can then be transitioned to routine thermal care. If the baby meets criteria for therapeutic

hypothermia, passive cooling is continued until the arrival of the transport team (Fairchild,

Sokora, Scott, & Zanelli, 2010).

Plan Following Discharge

Feeding Management

1. Continue to monitor M.P.’s intake.


2. Continue to monitor weight gain.

3. Follow with occupational therapy should feeding problems develop.

Development

1. Monitor developmental milestones

2. Monitor for functional difficulties well into school age.

2. Referral to Early Childhood Intervention, should deficits be noted.

3. Refer to occupational or physical therapy if problems are noted.

Seizure Management

1. Continue maintenance dose of Keppra for prevention of seizures.

2. Follow-up with pediatric neurologist.

Referrals

1. Pediatrician in M.P.’s home town.

2. Pediatric neurologist for seizure medication management.

3. Early Childhood Intervention for family assistance in long-term management.

Rationale: When functioning in the role of care provider, the DNP must assist in coordinating

multidisciplinary care for the complex pediatric patient.

Anticipatory Guidance

1. Follow with general pediatric healthcare provider for routine wellness examinations.

2. Recommended 2 month immunizations.

3. Seasonal vaccines for patient and family.

4. Parent teaching regarding basic growth and development. Establish understanding of

normal physical, cognitive and emotional expectations of M.P.


Rationale: The DNP must treat the whole patient, to include basic treatments and

teaching, assuring optimal growth and development. As M.P. ages, she will be expected

to reach specific developmental, functional, and social milestones. Teaching the parents

about these expectations allows them to recognize irregularities, should they appear

(Feigelman, 2007).

Family Support

Patient Handouts:

1. Hypoxic-Ischemic Encephalopathy (HIE) and Selective Head Cooling with the

Olympic Cool-CapR System Parent Frequently Asked Questions (see Appendix).

Rationale: The Doctor of Nursing Practice (DNP) must provide high quality, reliable

information for patients and families. The DNP must take into consideration the reading

literacy and health literacy levels in order to offer understandable information to

patients. The DNP should provide hard copies of documents, if the family does not have

access to the internet (United States Department of Health and Human Services, 2008).

Referral to Early Childhood Intervention

Rationale: ECI is a service provided through the Texas Department of Assistive and

Rehabilitation Services (2007). ECI provides no-cost services for those patients enrolled

in Medicaid. Programs are available for patients with cognitive, motor, communicative,

and social-emotional difficulties. M.P. is at risk for developmental, motor, functional,

and learning disabilities.


References

Anderson, M.E., Longhofer, T.A., Phillips, W., McRay, D.E. (2007). Passive cooling to initiate

hypothermia for transported encephalopathic newborns. Journal of Perinatology, 27:

592-593.

Fairchild, K., Sokora, D., Scott, J., & Zanelli, S. (2010). Therapeutic hypothermia on neonatal

transport: 4 year experience in a single NICU. Journal of Perinatology, 30:324-329.

Feigelman, S. (2007). The first year. In R. Kleigman, R. Behrman, H. Jensen & B. Stanton

(Eds.), Nelson textbook of pediatrics, (18th

ed., pp. 43-48). Philadelphia: Saunders

Elsevier.

Gluckman, P. D., Wyatt, J. S., Azzopardi, D., Ballard, R., Edwards, A.D., Ferriero, D.M., Polin,

R.A., Robertson, C.M., Thoresen, M., Whitelaw, A., & Gunn, A.J. (2005). Selective head

cooling with mild systemic hypothermia after neonatal encephalopathy: Multicentre

randomized trial. The Lancet, 365: 663-670.

Long, M., & Brandon, D., (2007). Induced hypothermia for neonates with hypoxic-ischemic

encephalopathy. Journal of Obstetric, Gynecologic, and Neonatal Nursing, 36 (3): 293-

298.

Olympic Cool-Cap System: Selective head cooling. (2009). Natus Medical Incorporated.

Retrieved from http://www.natus.com

Shankaran , S. , Laptook , A. , Ehrenkranz , R. , Tyson , J. , McDonald , S. , Donovan , E ., et al .

( 2005 ). Whole-body hypothermia for neonates with hypoxic-ischemic encephalopathy .

NewEngland Journal of Medicine , 353 , 1574 - 1584.

Texas Department of Assistive and Rehabilitation Services (2007). What is ECI? Retrieved from

http://www.dars.state.tx.us/ecis/index.shtml


United States Department of Health and Human Services. (2008). Health literacy improvement.

Office of Disease :Prevention and Health Promotion: Health Communication Activities.

Retrieved November 12, 2009, from http://www.health.gov/communication/literacy/

Volpe, J. J. (2008). Hypoxic-ischemic encephalopathy: Clinical aspects. Neurology of the

newborn (5th

ed., pp. 414-460). Philadelphia: Saunders Elsevier.

Von Gortand, A., Arnold, D., Adis, B. (1988). Posterior fossa hemorrhage in the newborn

period-diagnosis and management. Pediatric Radiology, 18: 347-348.

Zanelli, S., Stanley, D., & Kaufman, D., (2009). Hypoxic-Ischemic Encephalopathy. Retrieved

from http://emedicine.medscape.com/article/973501


Appendix

Hypoxic-Ischemic Encephalopathy (HIE) and Selective Head Cooling with the

Olympic Cool-CapR System

Parent Frequently Asked Questions

Your baby has a condition called hypoxic-ischemic encephalopathy (also abbreviated as HIE).

HIE is the term used to describe the condition whereby your baby’s brain has been deprived of

oxygen, before and/or during delivery. The seriousness of this condition is based on how long

his/her brain was without oxygen, the affected region of your baby’s brain, and the maturational

state of his/her brain cells.

HIE is a progressive injury that can develop over the next few hours to days. There are three

categories of HIE; mild, moderate, and severe. Most babies with mild HIE will recover with no

disability. Approximately 40-70% of babies with moderate HIE have some form of lifelong

disability such as cerebral palsy, cognitive deficits, and/or seizures. The most severe cases

almost always result in severe disabilities or death. Severe disabilities may include mental

retardation, severe motor dysfunction, and/or seizures.

What can be done to treat HIE?

Traditionally, babies with HIE were treated with supportive care: help breathing with a

ventilator, management of blood pressure, and/or management of seizures. There was no other

approved treatment for HIE. The Food and Drug Administrations (FDA) has now approved the

Olympic Cool-Cap System for the selective head cooling treatment of neonatal HIE.

What is selective head cooling and the Olympic Cool Cap System?

Science has shown that if your baby’s brain can be cooled down below normal body (normal

body temperature = 37o C) temperature (hypothermia) within 6 hours of birth, and their body

temperature kept in a consistent hypothermic range of 34oC to 35

oC for 72 hours, the Cool-Cap

system may interrupt the evolution of progressive damage to your baby’s brain, and may reduce

or prevent significant disability or death. While your baby’s head is kept cool, the rest of his/her

body will only experience mild hypothermia and will actually receive some warmth through the

radiant warmer. Because your baby’s head is kept cooler than the rest of his/her body, the

technique is called selective head cooling.

The Cool-Cap system uses a sealed water cap and two insulating caps placed over your baby’s

head. The temperature of the water cap is adjusted up or down to maintain the core body

temperature in the hypothermic range of 34oC

to 35

oC for the treatment duration. Once the

cooling treatment is complete, there is a 4-hour rewarming period. The water cap is removed

and the baby is allowed to slowly warm back up to a normal temperature. Your baby’s nurse

will carefully monitor your baby during the entire treatment to ensure his/her core temperature

remains in the target temperature range during the cooling treatment.

Olympic Medical, a Natus company 1 of 2 60099-FLF-EN0405R


What are the side effects of selective head cooling with the Olympic Cool-Cap System?

There are two expected, benign side effects associated with selective head cooling with the Cool-

Cap system, although not all babies will experience these side effects. The first is called minor

cardiac arrhythmia. A cardiac arrhythmia refers to an abnormality in the rhythm of your baby’s

heartbeat. The specific minor cardiac arrhythmia is called sinus bradycardia (a slow heartbeat)

and it is known to be associated with hypothermia.

The second side effect is head or scalp edema. Edema means swelling. This condition generally

goes away y itself, or with scalp massage or re-positioning. During the 72-hour treatment with

the Cool-Cap system, your baby’s nurse will regularly check under the water cap and around the

chinstrap to make sure there is no skin breakdown.

Does the Olympic Cool-Cap System cause my baby pain?

No. The Cool-Cap system is completely non-invasive.

What can I do to help my baby during the treatment?

It is extremely important that your baby rests during the entire treatment. You may stay with

your baby (per NICU guidelines), but try to keep your stimulation and interruptions to a

minimum. You can coordinate your interaction with your baby’s nurse to maintain the best

environment for your baby.

Your baby will not be fed via a bottle during the treatment. He/she will receive nutrition via an

intravenous (IV) line. Please continue to pump and store your breast milk.

Where can I find more information regarding HIE?

http://www.natus.com/

Olympic Medical, a Natus company 2 of 2 60099-FLF-EN0405R

CASE STUDY NEONATAL HEAD COOLING

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