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Head Cooling Information for Healthcare Professionals

The brain receives its energy supply from glucose and oxygen delivered through the cerebral circulation. Adenosine tri-phosphate (ATP) is produced and lactate, carbon dioxide, and water are produced as byproducts of oxidative brain metabolism. Hypoxic and ischemic brain injury can result from any disruption in delivery of vital glucose and oxygen to a part of the brain or to the entire brain. In neonates, events such as uterine rupture, placental abruption, or a tight nuchal cord can lead to a diffuse hypoxic brain injury and hypoxic-ischemic encephalopathy (HIE). Sometimes no such event is identified. Clinically, the neonates experience birth asphyxia, defined as a blood pH <7.00, along with elevated pCO2 and low pO2. The ensuing injury evolves over time.

There is a primary energy failure initially after the hypoxic event that leads to a small amount of necrotic cell death. Excitatory amino acids accumulate, there is cellular swelling, and high energy metabolites are consumed. The reperfusion period lasting around 30 minutes occurs during this time. There is then a latent phase lasting up to 24 hours in which the biochemical cascade leading to further neuronal injury is initiated.

During this time, the cerebral circulation and oxidative metabolism are somewhat normalized.

The secondary energy failure that follows leads to the majority of neuronal cell death through apoptosis. Here, there is accumulation of excitotoxins and failure of mitochondria. It is the severity of this secondary energy failure that is most correlated with a poor neurodevelopmental outcome.

Selective head cooling is initiated by 6 hours of life, during the primary energy failure in the latent phase and is continued through the time window when the secondary energy failure occurs. It therefore works to stop the biochemical cascade at multiple key points during a critical 72 hour period. The processes leading to necrotic and apoptotic cell death, mitochondrial failure, the toxicity produced by cytokines and excitotoxins are all reduced.

The head is cooled by the CoolCap device (Natus Medical Inc., San Carlos, CA, USA) set at 8-12°C to achieve a rectal temperature of 34.5 ± 0.5°C (Gluckman et al. 663-70).This tight temperature range is maintained for 72 hours and then the body is gradually re-warmed. An alternative method, used by some hospitals, involves whole body cooling with a cooling blanket for 72 hours (Shankaran S et al. 1574-84).The theoretical advantages offered by head cooling include less systemic side effects and the creation of a temperature gradient across the brain that adequately cools both the cortex and deep brain structures.


Gunn AJ. Cerebral hypothermia for prevention of brain injury following perinatal asphyxia. Curr Opin Pediatr 2000; 12:111-5.

Gunn A, Battin M, Gluckman P, Gunn T, Bennet L. Therapeutic hypothermia: from lab to NICU. J Perinat Med 2005; 33:340-6.

Gluckman P, Wyatt J, Azzopardi D, Ballard R, Edwards A, Ferriero DM, et al. Selective head cooling with mild systemic hypothermia after neonatal encephalopathy: multicentre randomized trial. Lancet 2005; 365: 663-70.

Mulkey SB, Yap VL, Kaiser JR. Strength in Numbers: Over 100 Infants with Neonatal HIE Cooled at Arkansas Children’s Hospital. Journal of the Arkansas Medical Society. 2012: 108(8):168-169.

Shankaran S, Laptook AR, Ehrenkranz RA, Tyson JE, McDonald SA, Donovan EF, et al. Whole-body hypothermia for neonates with hypoxic-ischemic encephalopathy. N Engl J Med 2005; 353(15):1574-84.

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