The use of mild therapeutic hypothermia as a means of neuroprotection has become an important treatment after cerebral hypoxic-ischaemic injury. Mild therapeutic hypothermia has been shown to improve outcome after out-of-hospital cardiac arrest and neonatal asphyxia, and several studies suggest a beneficial effect of mild therapeutic hypothermia on patient outcome after traumatic brain injury and cerebrovascular damage.
by Dr Oliver Kimberger
Management of mild hypothermia
Tiny reductions (> 0.2 °C) in core temperature trigger aggressive autonomic reactions – namely arterio-venous shunt vasoconstriction and shivering. However, there are several pharmacological agents which can lower the thermoregulatory thresholds and facilitate the induction of hypothermia. In particular, drugs used for general anaesthesia (volatile anaesthetics, opioids) lower vasoconstriction and shivering thresholds. This is the reason that the majority of patients undergoing treatment with mild hypothermia are anaesthetised and ventilated.
In contrast to other opioids, meperidine possesses additional anti-shivering action; the drug inhibits shivering twice as much as vasoconstriction. When used as a single drug in otherwise not anesthetised patients, high plasma concentrations are needed to reduce the shivering threshold to the desired temperature range of mild hypothermia. However, combinations of other anti – shivering drugs with meperidine mean that smaller doses of meperidine can be, while causing less patient sedation. Thus, with meperidine it is possible to achieve the cooling of conscious patients so that continuous neurological monitoring can be
carried out during hypothermia maintenance.
Another option to lower the shivering threshold and facilitate cooling is - paradoxically - skin warming. As the skin contributes approximately 20 % to the control of each thermoregulatory threshold, skin warming very efficiently lowers thermoregulatory thresholds without causing side effects. Obviously, skin warming is only possible, when invasive cooling (catheter or intravenous fluid cooling) is performed. Interestingly, skin warming does not significantly diminish invasive core cooling rates.
Cooling techniques
There are several methods to induce and maintain mild therapeutic hypothermia; some methods are focused on local cooling of cerebral tissue, but the majority aim at whole body cooling. Table 1 displays the most important cooling techniques:
Non-invasive cooling methods
Cooling with cold water mattresses is a common and widely used practice – yet not a very effective one since the back of the patient has only a relatively small contribution to overall patient heat transfer. Cold water mattress cooling works better, if the mattress is put on top of the patient like a blanket.
Cold air is a more efficient method to induce and maintain mild therapeutic hypothermia. For forced air cooling, room air is cooled to ≈ 10 °C in a blower device and delivered to the patient via a large hose into special blankets, or blown into a tent. Forced air cooling can be very effective, depending on the temperature of the air blown on the patient and on the strength of the blower.
Other efficient options for external cooling include the use of self-adhesive pads which circulate cold water [Figure 1]. The water in these pads is cooled according to feedback from a patient core temperature probe; the temperature of the pads can range between 4 °C and 42 °C. Other methods include the regional cooling of the head with cold helmets or a cap. A cap-system with circulating cold water is commercially available for the cooling of infants with hypoxic-ischaemic encephalopathy enabling brain cooling with less concomitant whole body hypothermia.
Invasive cooling methods
The rapid infusion of cold fluids is a very fast, cheap and tolerable method for the induction of mild therapeutic hypothermia.
A more invasive, yet very efficient method for induction and maintenance of mild therapeutic hypothermia is an intravenous cooling catheter system [Figure 2], inserted into the femoral vein or the subclavian / jugular vein using a Seldinger-technique. The cooling catheter has three lumina: one for the administration of medication or fluid. The other two lumina are connected to an external heat exchange system, and these two lumina join at the tip of the catheter. A core temperature input is used by the external heat exchanger device to control catheter temperature and maintain target temperature.
Monitoring of core temperature
Exact and reliable monitoring of core temperature is of high importance for the treatment of patients with mild therapeutic hypothermia, not least since many cooling systems rely on these core temperature measurements for their
feedback mechanisms.
Core temperature measurements can be obtained from many locations, however pulmonary artery temperatures remain the gold standard of core temperature thermometry. Alternative, but still feasible and fairly accurate locations for core temperature measurements include the distal oesophagus, nasopharynx, bladder and tympanic membrane. Mouth and rectum are less reliable core temperature measurement sites.
Rewarming
Rewarming can be performed with the very same device used for cooling (e.g. intravenous catheter, forced air, fluid pads). Sufficient evidence determining the optimal speed of patient core warming is still lacking – in general patients are warmed slowly and reach normothermia after 5 – 12 hours, and sometimes 24 hours, depending on the protocol applicable in the particular instiinstitution. Shivering and vasoconstriction also have to be treated during this time.
Complications of mild therapeutic hypothermia
Numerous studies have shown the association of accidental perioperative hypothermia with an increased incidence of complications. Naturally these findings also apply to mild therapeutic hypothermia: mild accidental hypothermia increases blood loss and the incidence of wound infections. In a prospective, randomised trial the wound infection rate doubled in mildly hypothermic patients. Hypothermia facilitates the development of wound infection via decreased tissue oxygen tension and impaired cellular immune response. Finally mild hypothermia increases the incidence of morbid cardiac events and dysrhythmias.
There are currently no absolute contraindications to mild hypothermia for neuroprotection, although the treatment may be relatively contraindicated in patients with coagulopathy, pregnant patients, patients with a high risk of wound infection and patients with severe dysrhythmias.
Conclusions
There are several feasible and affordable methods available to implement mild therapeutic hypothermia in any emergency room or intensive care unit. In summary, it is not yet possible to provide a unique recommendation for an optimal, specific cooling method or a particular medical sedation regimen — future clinical studies are needed to establish such optimised hypothermia treatment procedures and to discover new indications for mild therapeutic hypothermia.
The author
Oliver Kimberger, M.D.
Department of Anesthesiology,
General Intensive Care and Pain Medicine
Medical University of Vienna,
Austria
email: study@kimberger.at
