An incomplete epidemiological survey showed that during the summer heat wave abroad, the incidence of HS was 17.6–26.5 per 100,000 people, the hospital mortality rate was 14%-65%, and the ICU patient mortality rate was > 60% [5]. At present, the exact pathogenesis of severe heat stroke-related multiple organ dysfunction is not fully understood [8, 9], including the direct cytotoxic effects of high temperature and activation of sepsis-like inflammation cascades. Severe heat stroke damages the function of multiple organs throughout the body. The clinical manifestations mainly include: central nervous system damage (consciousness, mental disorders, cerebral edema, seizures, etc.), coagulation disorders (diffuse intravascular coagulation, prolonged coagulation time), liver and kidney Dysfunction, rhabdomyolysis, respiratory failure and cardiovascular complications (arrhythmia, hypovolemic shock) cause changes in the corresponding system detection indicators [10]. The severity of organ tissue damage is directly proportional to the prognosis [11]. At present, there is no unified standard for the diagnostic indicators of HS, and there is no specific method for evaluating the prognosis of HS. Leon LR [12] and others believe that a single systematic research indicator or score does not fully evaluate the interaction between multiple factors, and the prognosis of heat stroke is not Completely reliable. We analyzed more than two thousand data collected from 70 critically ill hospitalized patients. According to the severity of heatstroke, the patients were divided into three groups: control group (heat cramps and heat exhaustion), EHS, and CHS to compare the differences of indicators in each group. Try to find the test indicators that can judge the prognosis of severe heatstroke, and it can be carried out in clinic effectively, simply and quickly.
Among the 70 patients with severe heatstroke, 46 were males (65.7%) and 24 were females (34.3%); they were 22–96 years old, with an average age of (65.72 ± 16.64) years old. Considering that there are more men than women doing outdoor work in summer, the time and labor intensity of high temperature exposure are higher than women, but there is no statistical difference between men and women in each group (P > 0.05). we found that there were differences in body temperature in the mechanical ventilation group, combined with higher body temperature. High fever can cause hyperventilation and rapid respiratory rate. In foreign animal experiments, it has been found that the respiratory rate of pigs in severe heat stroke models is significantly faster than normal, suggesting that respiratory frequency may be an influencing factor for the prognosis of severe heat stroke [13].
We found that most of the patients with severe heat stroke in the above group have differences in liver function. Due to hypoxia and direct heat damage, the liver is found to be the most vulnerable organ. Liver transaminase is a very sensitive indicator of organ damage. Serum creatinine and blood urea nitrogen did not increase with the degree of damage. Previous data believe that the liver is the main site of heat damage, and most patients with heat stroke have liver tissue damage [14, 15]. Wagner M et al. [16] believed that the prognosis of patients with abnormal liver function due to heat stroke is extremely poor. A1zeer AH [17] found that serum ALT and AST increased during heat stroke, which can be used as an important reference index for the judgment and prognosis of heat stroke. We further analyzed that there was no statistical difference in liver function damage among severe heatstroke patients, suggesting that liver function may be an influencing factor for the onset of heatstroke, not a risk factor for prognostic assessment.
The APACHEⅡ score is currently a commonly used clinical evaluation system for critical illness. It consists of the sum of acute physiology, age, and chronic health conditions [18]. The highest theoretical score is 71 points, the higher the score, the more severe the condition. Studies have found that the APACHE II score is closely related to the severity of heatstroke, the higher the score, the more severe the disease [19, 20]. This study found that the APACHE Ⅱ score of the CHS group was higher than that of the control group, suggesting that the APACHE Ⅱ score has a certain significance for the prognosis of CHS, while the EHS score is lower than that of the control group. Considering that CHS patients are mostly elderly with underlying diseases, the general condition at the time of admission Poor, higher score. It was further found that the specificity and sensitivity of APACHEⅡ score were 0 and 85.71%, respectively, and the specificity was low. The AUC was 0.512, and the 95% confidence interval was 0.390–0.634. It suggests that APACHEⅡ is not of high predictive value in evaluating the prognosis of severe heat stroke.
In previous studies, serum PCT is a relatively specific marker of severe bacterial infection and sepsis [21]. Tong Hua sheng [22] compared the positive rate of serum PCT and blood culture in EHS and sepsis patients, and found that the PCT level and positive rate of blood culture in the EHS group were higher than those in the sepsis group. They believed that for EHS patients with elevated PCT, combined with blood culture and clinical analysis, in patients with significantly elevated serum PCT levels or patients with positive blood cultures, even if no direct focus of bacterial infection is found, active anti-infective treatment should be adopted. In our study, we collected the PCT of severe heatstroke patients. The PCT of the EHS group and the CHS group were higher than those of the control group, especially in the EHS group. In the middle and late stages of the disease, 25 patients developed systemic infections, mainly the following respiratory tract infections (EHS :12 vs CHS:9). PCT reflects the active degree of systemic inflammation, and its production is affected by many factors. Even if there is no bacterial infection or bacterial lesions, there will be obvious abnormalities. Therefore, we believe that a significant increase in PCT can greatly reflect the severity and prognosis of HS.
In the study, the DD of the EHS group was significantly higher than that of the control group and the CHS group (all P < 0.05); the PLT of the EHS group was significantly lower than the control group and the CHS group (all P < 0.05). Coagulation dysfunction is also involved in the important pathological process of severe heat stroke [23, 24]. Studies have shown that abnormalities in platelet and coagulation function can reflect the severity of severe heat stroke. The application of anticoagulant therapy may help improve the survival rate of patients [25]. The current abnormalities in the blood coagulation mechanism caused by heat stroke may be related to the direct cytotoxic effect of thermal stimulation and the cellular inflammatory response induced by thermal stimulation, which leads to vascular endothelial damage and micro thrombosis [26–27]. In addition, thermal stimulation can cause platelet aggregation, decrease in number, and consumption of coagulation factors, thereby inhibiting bone marrow production and releasing platelets [28–30].