Immediate postoperative fever following scoliosis surgery is rarely reported in the literature, which focuses predominantly on infectious [3, 7] and noninfectious [1, 4, 8] postoperative fevers occurring 24 to 72 h after surgery. The risk factors, treatments and prevention of immediate fevers in postoperative patients require analysis.
Postoperative fever presents as an increased body temperature higher than 38°C and is considered a common event that might complicate postoperative treatment ; there may not be an association between atelectasis and fever . Increasing evidence indicates that postoperative fever is an inflammatory response to surgical trauma to tissue resulting from the release of cytokines, such as interleukins 1 and 6, tumor necrosis factor-α, and interferon-γ, which affect the thermoregulatory mechanism at the hypothalamus; nevertheless, infection is an uncommon cause of postoperative fevers following posterior spinal fusion [4, 5]. The metabolic rate at which organisms transform energy and materials is largely governed by the Boltzmann factor, which describes the temperature dependence of biochemical processes, and the quarter-power allometric relation, which describes how biological rate processes are scaled according to body size . However, despite these indicators, when patients develop postoperative fevers, nearly all surgeons seek to rule out the possibility of an infection [7, 12]. In our case, there were clinical symptoms of immediate chills and fevers, but there was no evidence of a preoperative or postoperative inflammatory response to bacterial infection from any source during the over three-year follow-up period. We ruled out the possibility of an acute intraoperative infection or delayed infections, which may involve transfusion-related acute lung injury or septic transfusions [13, 14], as well as clinical symptoms with any suspected infection .
After ruling out an infection during the acute phase of a fever, the physician treating a patient with fever should consider the duration of the surgery and the inflammatory response that may be caused by surgical tissue trauma . An observational study found that nonpathological fevers commonly occurred 6.5 ± 3.01 days postoperatively . This evidence is not consistent with the case presented here. Therefore, we ruled out the possibility of a traumatic inflammatory response.
Intraoperative autologous transfusion may result in hemolysis during collection and hemoglobinuria and coagulation abnormalities after transfusion according to a two-case report from a previous study , and a retrospective observational study reported that 11% of patients in whom postoperative cell salvage was used experienced fever (> 38.3°C) or a chilly sensation immediately after the reinfusion of blood procured by postoperative cell salvage in 321 spinal surgeries without scoliosis . In our case, 750 ml and 300 ml of blood were transfused from intraoperative autologous and homologous transfusion, respectively, but there were no signs of hemolysis, hemoglobinuria or coagulation abnormalities following the transfusion. Although the intraoperative autologous blood was washed to separate red blood cells before reinfusion , it was reported that autologous blood was uniquely associated with a fever reaction in 11% of the patients receiving postoperative cell salvage rather than intraoperative autologous transfusion . Therefore, we could not rule out the possibility that these symptoms are due to transfusion reactions.
General anesthesia is considered to impair thermoregulation and to synchronously reduce the thresholds for vasoconstriction and shivering . Thermoregulation is inhibited to varying degrees during general anesthesia . The effect of general anesthesia on the inhibition of the thermoregulatory defense mechanism is dose dependent and can result in perioperative hypothermia. The intraoperative vital signs record show that the lowest body temperature (35.5°C) occurs on during 30 minutes after operation started. During recovery from anesthesia, patient symptoms (including shivering thermogenesis, increased heart rates, and increased blood pressure) are heightened, and postoperative fever may be related to temperature loss via inhibition of temperature regulation and exposure of large intraoperative incisions [18, 20, 21]. The differential diagnosis of malignant hyperthermia (MH) does not have a clear physiological mechanism, although skeletal and muscle metabolic abnormalities and hypothyroidism are associated with anesthesia. Considering human genetic susceptibility along with how abnormal chromosomal genetics affect MH, anesthesia is a factor that can cause skeletal muscle stiffness, high metabolism and high fever; if not immediately treated, tissue damage or death can occur . The diagnosis of MH is mainly based on indicators such as hyperpyrexia (> 40°C), hyperlactic acid and increased PaCO2 [23, 24]. In our patient, the arterial blood gas analysis results did not support the diagnosis of MH. In addition, glucocorticoid intervention may have been safe in our case  because the body temperature gradually returned to normal as time passed until the patient was discharged. Therefore, we reasoned that the symptom of immediate postoperative fever may be a self-limiting or self-regulating process, and there seemed to be no long-term adverse outcomes in our case with over three years of follow-up.
Postoperative tachycardia and hypertension are more frequent after general anesthesia . In our case, the heart rate and blood pressure immediately increased at the beginning of anesthesia recovery; general anesthesia was a risk factor that impacted hemodynamic stability in patients with posterior lumbar surgery, with cytokines being the most important group of inflammatory mediators, as they regulate the alterations that are evident in hemodynamic, metabolic and immune responses . Previous animal mechanistic research on sheep found that small doses of endotoxins evoked a dramatic biphasic response of opioid peptide secretion into the blood. The first phase began within minutes and coincided with a brief hypertensive response to endotoxins well before the appearance of fever or hypotension. In addition, the late increases in cerebrospinal fluid iβ-EP after endotoxin administration suggest that physiological stimuli such as fever, which provoke an outpouring of iβ-EP into the periphery, may occur along with changes in central opioid peptide metabolism . Based on this evidence, we consider general anesthesia to be a risk factor for fluctuations in hemodynamic stability.
In conclusion, immediate postoperative fever may be a self-limiting or self-regulating process in patients with scoliosis. The treatment intervention should be circumspect when patients experience such symptoms without clinical evidence because they may not have serious outcomes. Our case provides insufficient clinical evidence to determine whether this condition is due to transfusion reaction, or anesthesia inhibition.