In this section
Note: This guideline is currently under review.
Neonatal asphyxia is a major health issue globally. In developed countries asphyxia affects 3-5 per 1000 live births. Subsequent development of moderate to severe hypoxic-ischaemic encephalopathy (HIE) occurs in 0.5- 1 per 1000 live births., with up to 60% of these babies dying during the neonatal period and 25% of survivors having major long term neurodevelopmental problems.Many experimental animal models and systematic reviews of randomised controlled trials have shown that both whole-body hypothermia and selective head cooling has a neuroprotective effect. It modifies the cells programmed for apoptosis leading to their survival. Hypothermia may also protect neurons by reducing cerebral metabolic rate, attenuating the release of excitatory amino acids (glutamate, dopamine) improve the ischaemic impaired uptake of glutamate and lowering production of toxic nitric oxide and free radicals
Therapeutic hypothermia aims to lower the temperature of the vulnerable deep brain structures to 33-34°C.
Hypoxic-ischaemic Encephalopathy: Lack of sufficient oxygen to the brain and a diminished amount of blood perfusing the brain. This results in suppression of electrical activity and cortical depression.Primary Neuronal Death: immediate death if the insult is severe. This is related to cellular hypoxia leading to primary energy failure and cellular depolorisation.Secondary Neuronal Death: after a latent period (6-100 hrs) neuronal death may be initiated by a cascade of pathologic processes and is associated with marked encephalopathy. This involves cytotoxic oedema, mitochondrial failure, accumulation of excitotoxins, active cell death, nitric oxide synthesis and cytotoxic actions of activated microglia. Seizure activity is increased during this phaseEncephalopathy: Brain disease, damage or malfunction. In general encephalopathy is manifested by an altered mental state that may be accompanied by physical manifestations e.g abnormal limb movements.Apoptosis: Programmed cell death. Cells die in response to a variety of stimuli and during apoptosis they do so in a controlled, regulated manner. Apoptosis is a process in which cells play an active role in their own death and is often referred to as cell suicide.Medi-Therm III hyper/hypothermia system: Provides a means for regulating patient temperature by supplying temperature controlled water via a blanket placed under the patient.
Eligibility/criteria for therapeutic hypothermia
Constricted Bradycardia Periodic
heart rate apnoea
5. Moderate to severely abnormal background activity on amplitude-integrated EEG (.i.e. discontinuous, burst suppression or low voltage +/- seizure activity
6. At the neonatal consultant’s discretion to commence therapeutic cooling
The aim of cooling is to achieve the target temperature within 1 hour (rectal temperature between 33.0°C – 34.0°C)The total period of cooling and rewarming is for 84 hrs, consists of 2 phasesActive cooling- for 72 hours from the initiation of coolingRewarming- 12 hours of active gradual rewarming time after completion of 72hrs of cooling. Increase temperature by 0.5ºC every 2 hours as documented on care plan/treatment orders.
Set up and use of Medi-Therm III hyper/hypothermia system as per How to use Medi-Therm III hyper/hypothermia system.
Explain to family the reasoning for using hypothermia and the expected length of treatment. Explain to family that their baby will feel cold for the duration of the treatment and reassure them that their baby will be kept comfortable during the treatment. Encourage bonding by allowing parents to touch their baby, do nappy changes etc.
Notify doctor immediately if any of the above is observed, treat as per doctors orders.
How to use Medi-Therm III hyper/hypothermia system
Click here to view the evidence table for this nursing guideline.
Complete evidence table document available at http://www.wch.org.au/nursing/governance
Complete document control document available at http://www.wch.org.au/nursing/governance
Please remember to read the disclaimer.
The development of this nursing guideline was coordinated by Trudy Holton, Clinical Nurse Educator, Butterfly Ward, and approved by the Nursing Clinical Effectiveness Committee. Updated September 2014.