Neurol India Home 

Year : 1999  |  Volume : 47  |  Issue : 4  |  Page : 255--8

Hypothermia in craniocerebral trauma revisited.

M Sambasivan 
 Department of Neurosurgery, Medical College, Thiruvananthapuram, Kerala, 695011, India., India

Correspondence Address:
M Sambasivan
Department of Neurosurgery, Medical College, Thiruvananthapuram, Kerala, 695011, India.

How to cite this article:
Sambasivan M. Hypothermia in craniocerebral trauma revisited. Neurol India 1999;47:255-8

How to cite this URL:
Sambasivan M. Hypothermia in craniocerebral trauma revisited. Neurol India [serial online] 1999 [cited 2023 Jun 7 ];47:255-8
Available from:

Full Text

  ::   IntroductionTop

Management of craniocerebral trauma has seen many changes over the decades. Use of hypothermia aimed at brain protection was being employed in the seventies but was discarded due to attendant problems. This modality of treatment, however, is making a comeback in the recent years. A review of this procedure is thus warranted. In victims of craniocerebral trauma spontaneous hypothermia develops due to damage to hypothalamic areas concerned with thermoregulatory mechanisms. This requires separate consideration. Iatrogenically induced hypothermia is an accepted brain protecting measure.


Hypothermia as a therapeutic modality was used in modern medicine since 1950, with the experimental studies done by Bigelow.[1] Anaesthesia under hypothermia helped conducting open heart surgeries. Laugheed et al[2] in 1955 used hypothermia for brain protection. Body core temperature of less than 28 degree centigrade resulted in ventricular fibrillation, and thus further clinical application of this procedure was not pursued and it was relegated to bookshelves and oblivion.

Watanade in 1956 and Mohri in 1963 employed surface cooling to induce hypothermia and Higasa introduced it again with cardiopulmonary bypass in Japan. This led to the use of profound hypothermia and enabled tackling of highly vascular tumours or arterio venous malformations by neurosurgeons. This technique was used by Drake et al,[3] and many others for treating large vascular anomalies under profound hypothermia and total circulatory arrest. Rosomoff in 1959 noted the beneficial effects of hypothermia in craniocerebral trauma. However complications of hypothermia like electrolyte disturbances and changes in coagulation profile and infections precluded the use of hypothermia in neuratrauma. In 1970 barbiturate coma almost replaced hypothermia in brain protection. Kirino in 1982 noted the benefits of mild hypothermia in neurotrauma. Busto et al[4] noted reduction in ischaemic brain insult with hypothermia.

Miyagi et al[5] discussed the pitfalls associated with hypothermia and Bramlett et al[6] the protective effect of hypothermia in providing protection so that ischaemic effects are minimised. Clifton et al[7] in their study noted the use of moderate hypothermia in uncontrollable intracranial hypertension occurring after craniocerebral trauma. Marion et al[8] used moderate hypothermia in managing severe head injury with good results. Palmer et al[9] emphasised the cytoprotective effects of hypothermia by its effect in reducing the elevation of aspartate and glutamate. Use of mild hypothermia is now considered beneficial in the management of craniocerebral trauma as a brain protecting method.

Advantages of mild hypothermia ( 32o - 34oc ) :

1. Hypothermia tends to lower the intracranial pressure (ICP).

2. Hypothermia improves the CPP at temperatures of 32o to 34o centigrade.

3. Pyrexia in the traumatised patient adversely affects brain metabolism and this can be prevented by hypothermia.

4. Hypothermia reduces brain metabolism which protects the brain.

5 . Hypothermia prevents faster enzyme degradation seen at higher temperatures.

6. Hypothermia retards craniocerebral trauma induced ischaemic processes.

The disadvantages of hypothermia :

1. Hypokalaemia

2. Infections

3. Nursing problems

4. Skin and pressure points soddening

5. Energy requirements and nitrogen excretion greatly rises during rewarming, added nutritional support indicated.

Raised ICP produces a vicious cycle in which there is depression of respiratory activity with resultant hypoxia and hypercarbia, which further raise the ICP. Both hypoxia and hypercarbia excite the degeneration cascade of cellular activity. Extracellular levels of excitatory amino acids like glutamate and aspartate as well as dopamine increase, and this further affects the cellular activity in a detrimental manner.[10] Mild hypothermia is able to reduce this effect. Busto et al[4] noticed total inhibition of glutamate under mild hypothermia. Hypothermia reduces calcium influx into the cells as well as potassium efflux which are deleterious to the cell viability. Rapid depolarisation of neurones is also prevented under mild hypothermia.[11] Shapiro et al[12] have conclusively proved the beneficial effect of barbiturate augmented hypothermia for management of persistently raised ICP. Maintaining effect of pentobarbitone at 3 mg% and mild hypothermia could sustain ICP reduction upto five days without producing any cardiovascular instability or other side effects. This method could be employed in the management of cases of craniocerebral trauma, when cerebral oedema and raised ICP complicate the clinical picture.[12]

High dose of barbiturates render human body into a state of poikilothermia. Thus the combination of barbiturate and hypothermia may prove beneficial. Once the ICP has been reduced to acceptable levels of core temperature of 32o C, the barbiturate could be withdrawn. However, if the ICP remains elevated barbiturate augumentation could be continued. In these cases fall in blood pressure, decreased urinary output and gastric motility are to be treated on merits however, these are reversible on the discontinuation of hypothermia. Rewarming of the case must be done slowly to inhibit the rebound increase in ICP. The time taken for rewarming should be same as the cooling time. In severely traumatised patient, cerebral oxidative metabolism suffers. Consequently somato sensory evoked responses (SSEPs) deteriorate. This is attributable to the post traumatic ischaemia.[13] These effects can also be counteracted by hypothermia. Takeishi et al[14] proved the feasibility of hypothermia to control rise of ICP in craniocerebral trauma.

How to assess brain temperature? It is usually assumed that the brain temperature and core temperature are same. But this has been questioned.[15] To record the temperature the following sites are usually selected.

Site Reliability

1. Bladder Reasonable and possible

2. Rectum Reasonable and possible

3. Axila Fallacious

4. Oral Not useful in comatose

5. Oesophagus Considered better

6. Pulmonary artery Not always practicable

blood temperature

The brain temperature is higher than the tempertature recordable at all the points. [Right] lateral ventricle temperature was found to be 0.7 degrees higher than oesophageal temperature. When rectal temperature is 38oC, the brain temperature may be as high as 40oC. Thus during pyrexia in a patient with craniocerebral trauma the brain temperature would be at least 2 degrees higher than rectal temperature. This could prove deleterious to the neural tissue. Hence rise of temperature in a craniocerebral trauma patient must be treated aggressively to prevent the damage that would occur due to the rise of temperature. Here in lies the beneficial effect of mild hypothermia.

How to induce mild hypothermia ?

Mild hypothermia (32 to 34o C) can be achieved by :

1. Surface cooling using hypothermia blankets with cold fluid circulating through the blanket. Another method is to cover the patient with `ice bags'.

2. Venovenous cooling is done during the procedures using cardiopulmonary bypass. This is not employed in the routine cases in an I.C.U.

3. Gastric lavage with ice cold water or saline can also achieve hypothermia but the danger of fluid absorption and water intoxication is high. It, however, prevents hyperacidity and cushing ulcers.

In a survey conducted in US in 1997, 34% of board certified neurosurgeons recommend use of therapeutic moderate hypothermia in the management of severe head injury.[8] During the process of inducing hypothermia, continuous monitoring of patient's temperature using a rectal or oesophageal thermocouple is mandatory. It must be emphasised that surface cooling is the method of choice in the neuro ICU. If multiple ice bags are not available, plastic bags filled with water can be kept in the freezer after sealing the bags. This ice can be applied on the patient's body. Once the water thaws out, it can be reused. Plastic containers of saline can be frozen and used similarly. If conventional hypothermia units are not available these alternate methods described above can be usefully employed.

Water bed connected to a hypothermia unit can also be used. Patient's weight will push the water out into the cooling chamber. A pump with adjustable pressure force can push the cold fluid into the waterbed. The pumping pressure can be adjusted as per the needs dictated by the weight of the patient. This is my concept. The units could be manufactured here in India. The water bed mattress could be made of non-puncturable plastic and as a ripple mattress. Nursing the patient would be easy and pressure sores can be prevented. Coolant temperature can be adjusted by manipulating the temperature control knob kept on the coolant chamber. A digital recording of patient's temperature can be obtained from a thermistor probe kept in the rectum of patient and connecting it to a recorder in the hypothermia unit panel. This kind of a waterbed with all facilities would be ideally suited in a neuro ICU. Such beds avoid leakage of fluid and soddening of the back or pressure points. The same equipment can be used to rewarm the patient at the appropriate time by adjusting the coolant temperature. Thus mild hypothermia can be used to salvage even some of the devastated patients.

As mentioned earlier, cases of craniocerebral trauma may develop hypothermia due to damage of hypothalamic heat production centres. Interestingly this may be protecting the brain but further drop intemperature could complicate the system and the patient may develop cardiac irregularities. Such patient would need warming. In my experience with over 30,000 cases such instances were noticed in 14 cases, but timely recognition is important.

Twenty five years ago, it was the practice in our neuro ICU at Medical College Hospital to use hypothermia in every case of craniocerebral trauma with Glasgow Coma Scale (GCS) of 8 or less. The hypothermia units were available and were employed to give mild hypothermia. An approximate study was made but the results were not published because appropriate controls like measurement of hypothermia was not available. In all cases patient's temperature was recorded by a thermistor placed in the rectum and connected to a telethermometer. The data of 100 cases studied is mentioned in [Table I].

Let me conclude by emphasizing that:

1. Mild hypothermia has a role in the management of craniocerebral trauma.

2. Electrolyte fluctuations are minimal compared to deep hypothermia.

3. Prevention of fever is a positive point.

4. Appropriate physiotherapy reduces intercurrent infections.

5 . With newer designs the hypothermia blankets are better and produce less pressure.

6 . Better design of water beds would prove helpful.

7. Salvageability of cases with poor GCS grade is better.


1Kodama N, Asari J, Matsumoto M : History of hypothermia. Neurotraumatology 1997; 20 : 25-27.
2Lougheed WM, Sweet WH, White JC : Use of hypothermia in surgical treatment of cerebral vascular lesions. J Neurosurg 1955; 12 : 240-255.
3Drake CJ, Barr HWK, Coles JC : Extracorporeal circulation and profound hypothermia in the treatment of ruptured intracranial aneurysms. J Neurosurg 1964; 21 : 575-581.
4Busto R, Mardocoi BS, Globus YT et al : Effect of mild hypothermia on ischaemia induced release of neurotransmitters and free fatty acids in rat brain. J Cereb Blood Metab 1987; 7 : 729-738.
5Miyagi T, Tokutomi T, Morimoto K et al : Pitfalls of hypothermia in severe head injured patient. Neurotraumatology 1997; 20 : 28-32.
6Bramlett HM, Green EJ, Dietrich WD : Postischemic changes in brain hypothermia provides protection from sensorimotor or cognitive behavioural deficits. J Neurotrauma 1995; 12 : 289-298.
7Cliftoin GA, Allen S, Barrodale P : A phase II study of moderate hypothermia on uncontrollable intracranial hypertension after severe brain injury. J Neurotrauma 1993; 10 : 263-271.
8Marion DW : Management of traumatic brain injury, past, present and future. Clinical Neurosurgery 1997; 45 : 184-191.
9Palmer AM, Marion DW, Botscheller ML : Therapeutic hypothermia is cytoprotective without attenuating the traumatic brain injury induced elevations in concentrations of aspartate and glutamate. J Neurotrauma 1994; 10 : 363-372.
10Koizumi R, Fujisawa H, Ito H : Effect of mild hypothermia on cerebral blood flow, independent changes in cortical extracellular levels of amino acids following contusion trauma of rat. Brain Res 1997; 747 : 304-312.
11Sasahira S, Uchikado H, Miyagi N et al : Effect of mild hypothermia in rat. C.N.S. Neuron Neuratraumatology 1997; 20 : 83-86.
12Sapiro MH, Wyte SR, Loeser J ; Barbiturate augumented hypothermia for reduction of persistent intracranial hypertension. J Neurosurg 1974; 40 : 90-100.
13Jenifer IM, Brown MD, Moulton RJ et al : Cerebral oxidative metabolism and evoked potential deterioration after severe brain injury. New evidence of early post traumatic ischaemia. Neurosurgery 1998; 42 : 1057-1064.
14Takeishi A, Soejima Y, Tevira Y et al : Feasibility of titration method of mild hypothermia in severely head injured patients with intra cranial hypertension. Neurosurgery 1998; 42 : 1065-1070.
15Henker HA, Brown SD, Marion DW : Comparison of brain temperature with bladder and rectal temperature in adults with severe head injury. Neurosurgery 1998; 42 : 1071-1075.
16Fuse A, Yokota H : Effects of hypothermia in severe head injuries. Neurotraumatology 1997; 20 : 33-37.
17Shiozaki T, Sugimoto H, Tomida M : Effect of mild hypothermia in uncontrollable intracranial hypertension after severe head injury. J Neurosurg 1993; 79 : 363-368.