小儿发热及解热药的合理应用

发热是儿科最常见的临床症状之一，可出现于多种疾病中，如不及时治疗，极易引起高热惊厥等多种并发症，给儿童的身心带来一定影响。WHO建议，当小儿肛温高于38．5℃时，应采用安全的解热药治疗，对发热患者除对病因进行治疗外，选用安全有效的解热药也是不可忽视的问题。为此，本文就发热的概念及解热药的合理应用做一介绍。     

高热患儿物理降温存在的问题分析及护理对策

高热是儿科临床最常见的症状，是因为机体受到某种致热物质刺激后体温调节中枢的调定点上移，而出现体温过高的病理反映，体温一般在39℃以上。小儿的生理发育有其特点，年龄愈小，大脑皮质的发育愈不完善，愈易引起发热甚至高热。若高热持续过久，使体内调节功能失常，则影响小儿健康，严重时出现惊厥、昏迷，     

邱根祥教授治疗不明原因发热验案一则

<正>发热是小儿临床最为常见的临床症状,人体有一套完善的体温调节系统,在致热原的作用下或其他各种原因引起的体温调定点上移所造成的体温超出正常范围即为发热^[1]。发热虽不能作为一种单独的疾病,但其升降变化可准确地反映出疾病的转归和预后^[2]。     

发热的分子机制研究进展

发热是感染性或非感染性疾病触发的一种保守系统反应,它通过上调体温调定点引起体温升高.虽然,发热作为一种防御机制的结论 仍存在很多争议,但可确定的是,发热是临床患病的主要症状表现,是感染、炎症和中毒等疾病最早的报警信号之一.因此,从分子水平了解发热的基本机制,开发具有广阔前景的解热药具有重要的临床意义.     

暖风毯在小儿全身麻醉开腹手术中保暖的临床应用

<正>近年来随着小儿外科技术的不断发展,临床上开展长时间复杂手术亦是屡见不鲜,由于小儿皮肤薄、血管丰富、体表面积相对较大、小儿体温调节中枢发育尚不完善、体温调节能力相对较差,因此这些因素均造成小儿易于散热~([1-3])。围术期若不重视体温维护,则有可能让患儿产生与低体温相关并发症。暖风毯作为新型调温设备,对术中保温具有一定的功效~([4-6]),本文拟对暖风毯在小儿全身麻醉开腹手术中的临床应用价值进行探讨,现报告如下。     

我院门诊儿科处方中解药应用情况分析

发热是儿科最常见的临床症状之一,WHO建议当小儿肛温高于38.5℃时应采用安全的解热药治疗。对发热病儿除针对病因进行治     

常用退热药在儿科的选择应用

由于小儿免疫机制尚未发育成熟,比成人更易感染各种疾病,急性上呼吸道感染是儿科最常见的疾病之一,发热、咽痛、头痛为其主要症状。虽有资料说,对感染性疾病所致的发热在体温38．5～39．5℃时,对有良好的发病前背景和对发热能正常耐受的小儿来说,是机体有利于完善免疫应答的适应性反应,不需用解热药。但高热和长时间持续发热会对患儿造成不     

小儿高热的护理

体温是通过体温调节中枢来控制的,人体正常体温为36.3℃～37.2℃,超过37.3℃为低热,38.1℃～39℃为中度发热,39.1℃～41℃为高热,41℃以上为超高热。高热是儿科临床中最常见的急症,以六个月至六岁的小儿为主,当人体温度在41℃以上时,对人体的危害性很大,     

布洛芬与对乙酰氨基酚对小儿上呼吸道感染退热作用比较

发热是儿科最常见的临床症状之一，WHO建议当小儿肛温高于38．5℃时采用安全的解热药治疗。目前，市场上退热药物品种繁多，而临床上退热药物的选择存在较大的随意性、盲目性。为此，我院对上呼吸道感染（简称上感）发热患儿分别用布洛芬与对乙酰氨基酚进行退热治疗，现总结报告如下。     

小儿急性呼吸道感染应合理用药

小儿急性呼吸道感染是小儿最常见的疾病 ,如不及时治疗 ,常引起严重后果。据世界卫生组织调查表明 ,呼吸道急性感染引发的肺炎是发展中国家 <5岁儿童死亡的主要原因 ,在我国也是儿童死亡的第一原因。1　不合理用药情况呼吸道感染常伴有发热 ,一般家庭常自用一些解热药和抗菌药物 ,以为这样可以控制 ,其实这样用药是不太合理的。小儿呼吸道感染分为细菌感染和病毒感染 ,而后者占大多数。抗菌药对病毒不起作用 ,盲目应用反而会引起细菌耐药性的产生和发生不良反应。解热药只能解除临床发热症状 ,却不能杀死或抑制细菌与病毒的繁殖 ,用后反而掩…     

THERMOREGULATION IN RATS EXPOSED PERINATALLY TO DIOXIN: CORE TEMPERATURE STABILITY TO ALTERED AMBIENT TEMPERATURE,BEHAVIORAL THERMOREGULATION,AND FEBRILE RESPONSE TO LIPOPOLYSACCHARIDE

Recent studies have shown that perinatal exposure to 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD, dioxin) alters thermoregulatory function in adult rats and hamsters, indicated by a reduced body temperature during the animal's nocturnal phase. The present study was designed to assess the behavioral thermoregulation, ability to develop a fever, and thermoregulatory stability as a function of ambient temperature (Ta) in rats exposed perinatally to TCDD. Pregnant Long-Evans rats were exposed on gestational day (GD) 15 to 1 mug TCDD/kg (po). The male offspring were implanted with transmitters to monitor core temperature (Tc) and motor activity (MA). The 24-h pattern of core temperature was affected by TCDD exposure, characterized by a reduced nocturnal Tc. At some ages, the diurnal Tc of the TCDD group was elevated. This dysfunction in temperature regulation was most apparent at 7 and 11 mo of age. The 24-h pattern of MA was also altered by TCDD. The hypothermic effects of TCDD were most pronounced at cooler T values a of 10 to 22 C. In contrast, behavioral thermoregulation, assessed by measuring the selected Ta and Tc of rats in a temperature gradient, was unaffected by TCDD. The ability to develop a fever following administration of lipopolysaccharide (LPS) endotoxin (Escherichia coli; 50 mug/ kg) was accentuated in the TCDD-treated animals. The data confirm a nocturnal hypothermia in rats prenatally exposed to TCDD. However, the normal behavioral regulation of Tc suggests that hypothalamic thermoregulatory centers are not permanently altered. The accentuated fever in TCDD animals shows possible functional alterations in the neuroimmune and/or thermoregulatory axes involved in fever.     

The behavioral thermoregulatory response of febrile female rats is not attenuated by vagotomy

An oft-overlooked consequence of fever is the occurrence of thermoregulatory heat-seeking/producing behaviors. Subdiaphragmatic vagotomy attenuates fever resulting from low dose, peripherally administered pyrogens, suggesting that the vagus is involved in generating the pathogen-induced rise in core body temperature (T(c)). This study was designed to confirm that rats utilize behavioral thermoregulation to augment fever following systemic administration of lipopolysaccharide (LPS), and to test the hypothesis that, in febrile animals, vagotomy would block the preference for a higher ambient temperature (T(a)) as T(c) is rising. First, female Sprague-Dawley rats received IP injections of either saline or LPS (50 microg/kg), prior to placement inside a thermal gradient that offered subjects T(a) values between 7 and 45 degrees C. LPS injection caused significant increases in T(c) and selection of a higher T(a) as compared to saline administration. Second, groups of rats were vagotomized, sham-vagotomized or received no surgery, and then underwent the same gradient testing procedure. Vagotomy attenuated LPS-induced fever, but did not influence the concomitant behavioral thermoregulatory response. All groups selected comparable, higher T(a) values following LPS vs. saline. These data suggest that the reduction in the febrile response to LPS administration following vagotomy is not due to inhibition of the behavioral thermoregulatory response to the pyrogen. Rather, this behavioral response to LPS appears to be mediated by a nonvagal mechanism.     

Thermoregulatory responses to environmental toxicants: the interaction of thermal stress and toxicant exposure

Thermal stress can have a profound impact on the physiological responses that are elicited following environmental toxicant exposure. The efficacy by which toxicants enter the body is directly influenced by thermoregulatory effector responses that are evoked in response to high ambient temperatures. In mammals, the thermoregulatory response to heat stress consists of an increase in skin blood flow and moistening of the skin surface to dissipate core heat to the environment. These physiological responses may exacerbate chemical toxicity due to increased permeability of the skin, which facilitates the cutaneous absorption of many environmental toxicants. The core temperature responses that are elicited in response to high ambient temperatures, toxicant exposure or both can also have a profound impact on the ability of an organism to survive the insult. In small rodents, the thermoregulatory response to thermal stress and many environmental toxicants (such as organophosphate compounds) is often biphasic in nature, consisting initially of a regulated reduction in core temperature (i.e., hypothermia) followed by fever. Hypothermia is an important thermoregulatory survival strategy that is used by small rodents to diminish the effect of severe environmental insults on tissue homeostasis. The protective effect of hypothermia is realized by its effects on chemical toxicity as molecular and cellular processes, such as lipid peroxidation and the formation of reactive oxygen species, are minimized at reduced core temperatures. The beneficial effects of fever are unknown under these conditions. Perspective is provided on the applicability of data obtained in rodent models to the human condition.     

The effect of 6-hydroxydopamine pretreatment on the metabolic response produced by endotoxin in rabbits

The thermoregulatory, effector processes were investigated in rabbits after treatment with 6-hydroxydopamine (6-OHDA) and lipopolysaccharide Escherichia coli (LPS). Pyrogen (1 microgram/kg, i.v.) produced a fever reaction resulting from stimulation of the metabolic rate and heat conservation responses. Pretreatment with 6-OHDA (3 X 500 micrograms, i.c.v.) reduced the metabolic as well as pyretic activity of pyrogen. It is suggested that stimulation of the thermoregulatory heat production which contributes to the febrile rise in body temperature is dependent on the intact adrenergic structures in the central nervous system.     

Effect of central and peripheral cholinergic antagonists on chlorpyrifos-induced changes in body temperature in the rat

Exposure to the organophosphate (OP)-based pesticide chlorpyrifos (CHP) in the rat results in an initial period of hypothermia lasting < 24 h, followed by a fever lasting 48-72 h. The purpose of this study was to determine how cholinergic pathways participate in the mediation of the thermoregulatory effects of CHP. The corn oil (CO) vehicle or CHP (25 mg/kg; p.o.) was administered to female rats while core temperature (Tc) and motor activity (MA) were monitored by radiotelemetry. The peripheral muscarinic antagonist, methyl scopolamine (MS) and central antagonist, scopolamine (S) were administered during the period of CHP-induced hypothermia and fever. The hypothermia was attenuated by scopolamine but not by methyl scopolamine. The delayed fever was augmented by scopolamine but blocked by methyl scopolamine. The results indicate that CHP-induced hypothermia is mediated by cholinergic stimulation of heat loss pathways in CNS thermoregulatory centers. Peripheral cholinergic pathways appear to have a minimal role in mediating chlorpyrifos-induced hypothermia. On the other hand, the chlorpyrifos-induced fever appears to be mediated by a peripheral pathway that is blocked by methyl scopolamine. The data provides a possible explanation for the persistent fever in humans exposed to OP pesticides and treated with atropine. Methyl atropine or methyl scopolamine may be a more effective therapy in the treatment of the fever.     

Experimental Biology 1997 Symposium on Neurobiology of Thennoregulation: Role of Stress: POISONS AND FEVER

1. Dysfunction of the thermoregulatory system is one of many pathologies documented in experimental animals and humans exposed to toxic chemicals. The mechanism of action responsible for many types of poison-induced fevers is not understood. Some elevations in body temperature are attributed to the peripheral actions of some poisons that stimulate metabolic rate and cause a forced hyperthermia. Exposure to organophosphate (OP) pesticides and certain metal fumes appears to cause a prolonged, regulated elevation in body temperature (Tb). 2. Activation of cyclo-oxygenase (COX) and the production of prostaglandin (PG)E₂ in central nervous system (CNS) thermoregulatory centres is required to elicit a fever. Activating the COX-PGE₂ pathway by a poison may occur by one of three mechanisms: (i) induction of cell-mediated immune responses and the subsequent release of cytokines; (ii) induction of lipid peroxidation in the CNS; and (iii) direct neurochemical activation. 3. Radiotelemetric monitoring of core temperature in unstressed rodents has led to an experimental animal model of poison-induced fever. Rats administered the OP agents chlorpyrifos and diisopropyl fluorophosphate display an initial hypothermic response lasting approximately 24 h, followed by an elevation in diurnal core temperature for 24–72 h after exposure. The hyperthermia is apparently a result of the activation of the COX-PGE₂ pathway because it is blocked by the anti-pyretic sodium salicylate. Overall, the delayed hyperthermia resulting from OP exposure involves activation of thermoregulatory pathways that may be similar to infectionmediated fever.     

Effects of chronic exercise conditioning on thermal responses to lipopolysaccharide and turpentine abscess in female rats

Chronic exercise conditioning has been shown to alter basal thermoregulatory processes as well as the response to inflammatory agents. Two such agents, lipopolysaccharide (LPS) and turpentine (TPT) are inducers of fever in rats. LPS, given intraperitoneally (i.p.), involves a systemic inflammatory response whereas TPT given intramuscularly (i.m.) elicits a localized inflammation. We assessed if chronic exercise training in the rat would alter the thermoregulatory response to LPS and TPT. Core temperature (T _c) and motor activity were monitored by radiotelemetry. Female Sprague Dawley rats were divided into two groups (trained and sedentary) and housed at an ambient temperature of 22°C. Animals voluntarily trained on running wheels for 8 weeks. In the first study, trained and sedentary female rats were injected i.p. with LPS (50 μg/kg) or an equal volume of 0.9% normal saline. In another study, trained and sedentary female rats were injected i.m. with TPT (10 μl)/rat or an equal volume of 0.9% normal saline. The time course of the LPS fever was very short compared to TPT. TPT injected animals displayed a smaller but more prolonged fever compared to LPS; however, training accentuated the febrile response to LPS (ΔT _c=0.6°C in sedentary and 1.2°C in trained). Training had a slight suppression on TPT-induced fever during the daytime but had no effect on motor activity or nighttime T _c. In contrast, exercise training led to a marked increase in the pyrogenic effects of LPS. We conclude that the effect of exercise training and source of infection (i.e., systemic versus localized in muscle) on fever is directly linked to type of pyrogenic agent.     

Molecular mechanisms in endotoxin fever

Two important concepts are presented in this review. First, endotoxin fever, like all fevers, is mediated by a host product, leukocytic pyrogen (LP). The mechanism by which LP production is initiated by endotoxin is discussed and evidence is provided which clearly distinguishes the biological and physical differences between LP and endotoxins. The second concept is that many of the molecular and neurochemical mechanisms by which LP causes fever by its action on the hypothalamic thermoregulatory center are also observed when endotoxins are introduced into the central nervous system. Thus, there may be experimental and clinical situations in which endotoxins can directly affect the hypothalamus and initiate fever. Although this bi-modal effect of endotoxin on the production of fever can occur, the importance of LP in mediating endotoxin and other fevers cannot be overstated.     

IgE-mediated drug fever due to histamine H2-receptor blockers

Drug-induced fever due to histamine H2-receptor blockers was experienced by a 55-year-old man. The patient became febrile 5 days after receiving cimetidine, and continued to be febrile until the drug was stopped. His maximum body temperature was above 40 degrees C. Challenge tests with cimetidine and ranitidine showed that the fever was caused by the H2-blocker. The patient's serum IgE concentration increased markedly to 2590 IU/ml 10 days after admission, and skin tests for cimetidine and ranitidine were positive. Lymphocyte stimulation tests were positive for both drugs (stimulation indices: 193% for cimetidine and 325% for ranitidine). Cimetidine-induced fever has generally been thought to be due to a direct effect on the thermoregulatory centre in the hypothalamus, on the basis of experimental studies of the injection of cimetidine to the cerebral ventricles. However, clinical evidence has not excluded an allergic involvement in this type of drug-induced fever. This patient's fever was proven to be due to administration of the H2-blocker, and the mechanism of action was IgE-mediated.     

Inhibition of pyrogen Escherichia coli fever with intracerebral administration of prazosin, dihydrobenzperidol and nifedipin in the rabbits

1. The thermoregulatory, effector processes were investigated after treatment with prazosin (PRA), dihydrobenzperidol (DHBP) and nifedipin (ADA) applied to the thermosensitive zone of the anterior hypothalamus (PO/AH) on normothermic and feverish rabbits (LPS, lipopolysaccharide E. coli; 1 meg/kg, i.v.). 2. The alpha 1-noradrenergic receptor antagonists, PRA and DHBP, applied to the PO/AH produced an abolishment of fever elicited by pyrogen i.v. injection mainly because of vasodilation of ear skin vessels and attenuation of metabolic rate. 3. Calcium channel blocker, ADA, also induced a decline in the rabbit's core temperature in the same manner. 4. All these drugs given to the PO/AH did not change the body temperature in normothermic rabbits. 5. These results, therefore, strongly suggest that alpha 1-noradrenergic receptors subserve the coordinated thermoregulatory mechanisms in PO/AH which are required for antipyresis. The inhibition of Ca2+ turnover is discussed as a possible mechanism of antipyretic action of these drugs given to the PO/AH.