Chills, produced by rapid rhythmic contraction of skeletal muscles, are a compensatory response of the body to hypothermia. Chills may be induced when the body temperature falls below the hypothalamic temperature in order to maintain body temperature homeostasis. Post-anesthesia chills, the first manifestation of peripheral vasoconstriction and a drop in central body temperature, that is, the so-called “idiopathic post-general anesthesia chills”, “thiopental-like tonic”.
A, the incidence of chills after anesthesia and the danger
The danger of chills.
1) The metabolic rate of the body is significantly increased, the body’s oxygen consumption increases, oxygen consumption is usually two to five times, while carbon dioxide and lactic acid production increases, the body through the strengthening of respiratory and cardiac work to obtain compensation, cardiopulmonary load therefore increases, for critically ill patients can lead to cardiopulmonary failure.
2) Dynamic electrocardiography confirms that the proportion of myocardial ischemia is significantly higher in patients with body temperature below 35°C than in those with normal body temperature.
3) Chills under hypothermia can impair platelet function, inhibit coagulation cascade reaction, significantly increase blood loss, and increase blood transfusion.
Second, the mechanism of post-anesthesia chills
1) The mechanism of post-anesthesia chills is not fully understood, Sessler study, the distribution of body heat can be divided into “central chamber” and “peripheral chamber”. The central chamber is rich in blood flow and its temperature is called “core body temperature”, which remains stable in a narrow range. The temperature of the peripheral chamber is more influenced by the external temperature, and there are large temperature differences between the various parts of the peripheral chamber. The heat between the central and peripheral chambers is in a dynamic state of change. Under normal conditions, the peripheral vasculature is constricted during cold and there is less heat pairing between the central and peripheral chambers, thus reducing internal heat dissipation to maintain a stable central chamber temperature. In the anesthetized state, the peripheral vascular contraction response to cold stimulation is diminished due to sympathetic nerve function blockade.
As a result, body heat is rapidly conducted from the central to the peripheral chambers (heat redistribution) and the central temperature rapidly decreases, thus stimulating the body’s temperature receptors and causing a chilling response. Core temperature decreased up to 0.8 ± 0.3°C within the first hour after anesthesia induction; redistribution of body heat accounted for 89%. In the following 3 h, the body temperature continued to fall by about 0.4±0.3°C, of which redistribution of body heat accounted for 62%. It can be seen that redistribution of body heat during anesthesia is an important factor in causing chills.
Rosenberg et al. suggested that chills after anesthesia are related to the speed of restoration of awakening of nerve centers at all levels after anesthesia, and the different sequences, with the spinal cord response center awakening earlier than the brain response center, resulting in spontaneous muscle tremors as a result of involuntary nerve reflexes. It is also believed that chills occur due to the dysfunction of the thermoregulatory center of the brain during the recovery process of anesthesia.
Third, the causes of post-anesthesia chills
There are many triggers of post-anesthesia chills, and it is not certain which is the exact factor that induces chills, but various triggers have some relevance to post-anesthesia chills.
1, the triggers of hypothermia.
Hypothermia can cause chills, cold can stimulate body surface temperature receptors and intracranial temperature neurons, while acting on the hypothalamic thermoregulatory center, prompting muscle tremors, increased cardiopulmonary activity, heat production, in order to maintain internal heat balance.
In 1986, Ponte proposed that the cause of chills in patients under epidural anesthesia was related to the stimulation of spinal cord temperature receptors by cold anesthetics, and Nishimura et al. showed that postoperative chills after general anesthesia were associated with a decrease in peripheral body surface temperature. The current study shows that the temperature of the local anesthetic, by itself, is not the cause of chills, and that epidural cavity injection of cold saline (17±2.2°C) does not cause chills. The results of the above studies are widely divergent, but there is general agreement that perioperative insulation of the body and prevention of hypothermia may avoid chills, or inhibit them. Input control and regulation of thermal information, which can affect the occurrence of chills, may be related to the reduced response of the brain center to cold during recovery from anesthesia, while the spinal cord center responds normally.
2. Pyrogenic factors.
During intraoperative blood and fluid transfusion, sudden chills and hyperthermia up to 38-41℃, accompanied by nausea, headache, pulse rate and other symptoms can occur, which is a thermogenic reaction caused by blood and fluid transfusion, and the latter can cause imbalance in the thermoregulatory center.
3. Patient factors.
Nishimura et al. showed that the incidence of chills after anesthesia was higher in younger patients than in older patients, and the protective mechanism of the body against hypothermia in younger patients was better than in older patients, which may be related to. 2595 cases of observation room patients were observed by Crossley, and it was found that the incidence of chills in male patients was significantly higher than in female patients; the incidence of chills in young and strong patients was higher than in pediatric and elderly patients. The occurrence of chills was not significantly related to patient height and weight.
4. Drug factors.
Crossley found that the preoperative use of anticholinergic drugs could reduce chills. Intraoperative application of alfentanil and pethidine can reduce chills. Goold reported that the incidence of chills was higher in patients who applied painkillers before surgery than in those who did not use painkillers; the rate of chills was lower in patients who were given Valium before surgery than in those who did not use it.
5. Hypoxia.
Intraoperative hypoxemia can be caused by a variety of factors, the latter of which can lead to hypoxic chills with headache, increased pulse rate, deep and rapid breathing, increased blood pressure and decreased PaO2. In severe cases, heart rate is slowed, respiratory depression, confusion, and even convulsions.
IV. Treatment of post-anesthesia chills
1.Pharmacological treatment
(1) Central excitatory drugs: the representative drug is [Doxapram], a central excitatory drug, to speed up the recovery of the brain from the inhibition of anesthetic drugs, thereby establishing normal control of the spinal cord reflexes, resulting in effective treatment of post-anesthesia chills. In a controlled study, the saline group (n=20), the pethidine group (0.3mg/kg,n=20) and doxapram (1.5mg/kg,n=20) were effective in treating chills in both the doxapram and pethidine groups after 2-3 minutes of intravenous administration, while 15 patients remained chilled after 10 minutes of administration in the saline group.
(2) Opioids: The representative drug is [pethidine], which produces the effect of chills control through excitation of μ and κ morphine receptors, mainly through excitation of κ receptors. claybon et al. used pethidine 0.4 mg/kg, and chills disappeared in 73% of patients with chills after anesthesia within 5 minutes.
(3) α2-adrenergic receptor agonist: The representative drug is [colistin], which has an anti-chilling effect after anesthesia, probably by inhibiting the thermoregulatory center of the brain, lowering the chilling threshold, and inhibiting temperature afferent information at the spinal cord level, thus inhibiting chills. In the colistin 75μg group, the chills disappeared at 100% 4 minutes after administration; in the colistin 150μg group, all chills disappeared within 2 minutes after administration. It showed that the efficacy of colistin in the treatment of chills was significant and positively correlated with the dosage.
(4) Tramadol: [Tramadol] mechanism of action: in the spinal cord segment, it has the effect of inhibiting 5-HT and norepinephrine reabsorption, attenuating opioid activity, and inhibiting pain signaling. 5-HT and norepinephrine play an important role in temperature control, but the effect of tramadol on temperature control remains to be elucidated. witte et al. confirmed in 72 adult patients that 1mg/kg Tramadol. It can prevent 100% of chills from occurring. Comparing the effects of tramadol and pethidine, it is believed that there is a synergistic effect between pethidine and the previously used opioids, which may have a risk of respiratory depression, while tramadol is safer and more effective.
2.Physical therapy
Sessler et al. took [skin heating] or no heating measures for patients under epidural anesthesia, resulting in a high incidence of chills and a significant decrease in tympanic membrane temperature in the no-heating group. sharkey observed 30 chills in patients treated with [radiant heat], 22 chills disappeared and 4 chills were reduced. It is generally accepted that keeping the patient warm by physical means or raising the ambient temperature can reduce cold information transmission and reduce and suppress chills.
V. Prevention of chills after anesthesia
First of all, pay attention to perioperative insulation, using thermal blankets, raising the operating room ambient temperature, heating and wetting inhaled gas during anesthesia, which can reduce heat dissipation in the trachea. Laying sheets as soon as possible after surgical disinfection to reduce the patient’s body temperature drop can prevent chills. Preoperative application of doxapram, colistin, or preoperative administration of sedatives can reduce post-anesthetic chills.