Hypothermia is one of the management strategies that are used in traumatic brain injury patients. Hypothermia occurs when the body’s core or internal temperature is 35oc (Smeltzer et al, 2010: 736). Some of the symptoms are severe shivering and feelings of cold and chills. Death may occur if normal temperature drops to 34oc (Kozier, 2002: 117). Hypothermia in traumatic brain injury patients will be discussed and debated including the negative and positive outcomes of using hypothermia as a management strategy.
Hypothermia is classified by (Dougherty et al, 2008: 656) as mild (32 – 35oc), moderate (28 – 32oc) and severe (less than 28oc). He further states that hypothermia causes the metabolic rate to decrease from a core temperature of 35oc and lower. Basically the body loses heat and is unable to maintain homeostasis (Dougherty, 2008: 656). Signs and symptoms of hypothermia is severe shivering, feeling of cold and chills, pale, cool, waxy skin, hypothermia, decreased urinary output, lack of muscle coordination, disorientation and drowsiness progressing to coma (Kozier, 2002: 117).
Pathophysiological consequences of hypothermia Hypothermia is closely linked with mortality and morbidity as the patients chances of survival dramatically decrease if the body’s core temperature is less than 34 0 c. The mortality and morbidity may however be due to impaired coagulation, metabolic acidosis because of poor perfusion of tissues, hemodynamic instability, respiratory problems and infection. A patient’s core temperature may also be altered during the initial evaluation and resuscitation leading to a poor prognosis in the injured patient (15790382: 116).
The human body contains ionotropic receptors. It is “a type of neurotransmitter receptor that has a neurotransmitter binding site and an ion channel” (Tortora, 2009: 443). This ion channel will only open when the correct neurotransmitter binds to the site causing either an excitatory postsynaptic potential or an inhibitory postsynaptic potential. Therefore, hypothermia causes a negative ionotropic effect on the myocardium, depresses the left ventricular contractibility and may also be associated with atrial and ventricular arrhythmias.
When the initial ecg of a patient is done, it will reflect sinus tachycardia patterns and as the core temperature drops even further the pattern changes to sinus bradycardia (15790382: 117). Intra-operative hypothermia may also increase the occurrence of cardiac incidences like myocardial ischemia, unstable angina and ventricular tachycardia. The increase in cardiovascular morbidity may be due to peripheral vasoconstriction, increase norepinephrine levels and changes in alpha – adrenoceptor tone in response to the decreased temperature.
Hypothermia can also contribute to surgical wound infection because of thermoregulatory vasoconstriction, reduced subcutaneous oxygen tension, reduction in collagen deposition and impaired oxidative killing by neutrophils. Hyperglycaemia may occur, which will require intensive insulin therapy to decrease the chances of mortality, and the patient may also have bleeding diathesis (15790382: 117). The role of therapeutic hypothermia in traumatic brain injuries Therapeutic hypothermia may have a protective function by decreasing oxygen consumption.
Bleeding should be stopped and fluids should be administered while keeping the patient in a close to normothermic state. In this study it was recorded that mild hypothermia during pre – hospital cardiac arrest, may protect the brain against anoxia when patients are resuscitated. “The Advanced Life Support task Force of the International Liaison Committee now recommends that unconscious adults with spontaneous circulation after out of hospital cardiac arrest should be cooled to 32 – 34oc for 12 -24 hours when the initial rhythm was ventricular fibrillation” (15790382 : 117).
This may be done by administering iced saline gastric lavage and placing ice packs under the axilla and groin area (Smeltzer et al, 2010: 736). According to (15790382), the role of therapeutic hypothermia is still being debated. The reason for the debate is because of the existence of methological issues like hypoxia or hypotension after resuscitation, when hypothermia therapy should be started and how long therapeutic hypothermia should be used.
Patients with intracranial hypertension should receive hypothermia therapy for more than 48 hours. At the end of the study (15790382) concluded that hypothermia may sometimes complicate the management of patients with severe blunt or penetrating injury and this may contribute to the increase in mortality and morbidity if bleeding and further heat loss is not controlled. If the former is prevented during the initial stage of the traumatic brain injury, the lethal triad of hypothermia, acidosis and coagulopathy can be avoided.
Therefore, “hypothermia is still considered a foe in these patients and on the other side accidental or induced hypothermia may be beneficial “a friend” in selected patients with traumatic brain injury” (15790382: 118). According to (15790382) the effect of prolonged hypothermia during resuscitation of a patient after haemorrhagic shock is still unclear. Therapeutic Hypothermia (19967463) stated that hypothermia in traumatic brain injury was noted from the time of the Hippocrates in the 460 – 377 BC.
It said that “a man will survive longer in winter than in summer, whatever be the part of the head in which the wound is situated” (19967463: 168). This meant that hypothermia may have a neuro – protective function but this is still being debated but is likely to be multi factional (19967463: 168). According to (19967463) in Rodent models, mild to moderate hypothermia will cause blood brain barrier dysfunction, cerebral oedema, reduce levels of excitatory neurotransmitters and free radical production and inflammatory responses.
It was shown that hypothermia decreases cerebral metabolic rate. For every 1oc drop in temperature there’s a 6 – 7% drop in cerebral metabolic rate due to this cerebral blood flow and cerebral blood volume may decrease ICP. “Hypothermia has been used both as a neuroprotectant, where it was induced as soon as possible after injury, and also to control increased ICP, where it was usually used as a second – tier therapy” (19967463: 168). Hypothermia for neuroprotection Preclinical studies were done and it found that mild to moderate hypothermia may improve survival and neurological outcomes.
It also showed that larger hospitals that had more experience in applying hypothermia to patients with traumatic brain injury had more favourable outcomes in this specific management. Further studies were done and it seems that late induction of hypothermia or complications also influenced the outcomes of the patients. The adverse effects of hypothermia include cardiac arrhythmias, coagulopathies, pulmonary infections, hypothermia – induced dieresis and electrolyte derangement (19967463: 168). (19967463) so during this study, they then applied a strict protocol to prevent the occurrences of these side effects.
For example they would use antiarrhythmics , checked the fluid balance frequently and this included electrolyte analyses. Eldar then came to the conclusion that people treated with hypothermia had a better outcomes than some treated with barbiturate – treated controls. He then did a study on patients who were receiving tramatic brain injury treatment with hypothermia. The optimal beneficial effects of hypothermia on intracranial pressure and indices of cerebral metabolism were observed at 35oc. At 35oc adverse effects are less likely to occur (15790382: 117).
Hypothermia for intracranial pressure control According to Eldar, in both laboratory and clinical studies, hypothermia seems to decrease intracranial pressure (ICP) in patients with severe traumatic brain injuries. Elder further stated that patients with an increase in ICP refractory, receiving barbiturates and patient has mild hypothermia (temperature about 34oc), there ICP was better controlled and improved short – term survival but patients who had induced mild hypothermia and low intracranial pressure (<25mmhg) had no advantages but there was an increase in systemic infections.
This meant that mild hypothermia can only be used in patients with ICP that cannot be controlled and not in patients with an ICP of less 25mmhg. At the end of this study it was concluded that “induced therapeutic hypothermia for traumatic brain injuries should not be as a blanket therapy of a fixed depth and duration. Instead, the depth and length of hypothermic therapy may not need to be varied depending on the severity of injury and the time from injury.
Titration to effect close attention to fluid balance and prompt fluid and electrolyte replacement may help minimize side – effects” (15790382: 117). Management in an acute care setting Effect In 1997, a randomized study was done to evaluate the effects of moderate hypothermia, which ranged between 32 – 33oc for 24 hours versus normothermia in patients suffering from severe traumatic brain injuries, taking into consideration that their Glasgow Coma Scale must be 5 – 7 and not lower. The results of this were that there was an improvement in the outcomes in the hypothermic group (11309068, 307).
Another randomized study was done on the same type of patients but the only difference is that they were evaluated with mild hypothermia for 3 – 14 days until ICP has decreased. The results recorded was that about 46, 5% of the hypothermic group had favourable outcome and the rest of the 27, 3% not so favourable (Jiang, 2000: 307). Then in a randomized controlled study, there were no clear benefits of the use of hypothermia nor did it show any significant systemic complication like coagulopathy (11309068, 307).
Conclusion The loss of body heat due to Hypothermia can lead to loss of consciousness or death in severe cases. Hypothermia is associated with mortality and morbidity and this may be due to the drop in body core temperature as well as increase the occurrences of cardiac incidences. Hypothermia contributes to surgical wound infection and increases the occurrence of hyperglycemia which may result in increased probability of mortality. By keeping the patient close to the normothermic state, Hypothermia may also protect the brain against anoxia.
Patients with intracranial hypertension can receive mild hypothermic theraphy given the ICP is more then 25mmhg. If Hyperthermia is applied soon after an injury, it may act as a neuroprotectant and assist in controlling the intracranial pressure. The outcome of this management strategy is proportional to the size and experience of the hospital. Outomes also depend on our soon hypothermia is induced after the injury. Optimal beneficial effects of hypothermia occur at 35oc. Studies also show that patients treated with hypothermia have better outcomes than some treated with barbiturate – treated controls