The hot patient: acute drug-induced hyperthermia

Jamshidi, Nazila; Dawson, Andrew

doi:10.18773/austprescr.2019.006

Cited by 16 publications

(13 citation statements)

References 17 publications

(16 reference statements)

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“…A wide variety of xenobiotics can affect the thermal homeostasis, triggering or exacerbating the hyperthermia-induced damage, both by the increased metabolic heat production (e.g., sympathomimetic agents) or by an impairment of heat-dissipating effector mechanisms (e.g., anticholinergic agents) [3]. This disruption will consequently affect many other homeostatic systems and may result in several life-threatening complications such as disseminated intravascular coagulation, hyperkalemia, metabolic acidosis, multi-organ failure, and rhabdomyolysis [4,5,6].…”

Section: Introductionmentioning

confidence: 99%

Hepatic Metabolic Derangements Triggered by Hyperthermia: An In Vitro Metabolomic Study

et al. 2019

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Background and aims: Liver toxicity is a well-documented and potentially fatal adverse complication of hyperthermia. However, the impact of hyperthermia on the hepatic metabolome has hitherto not been investigated. Methods: In this study, gas chromatography-mass spectrometry (GC-MS)-based metabolomics was applied to assess the in vitro metabolic response of primary mouse hepatocytes (PMH, n = 10) to a heat stress stimulus, i.e., after 24 h exposure to 40.5 °C. Metabolomic profiling of both intracellular metabolites and volatile metabolites in the extracellular medium of PMH was performed. Results: Multivariate analysis showed alterations in levels of 22 intra- and 59 extracellular metabolites, unveiling the capability of the metabolic pattern to discriminate cells exposed to heat stress from cells incubated at normothermic conditions (37 °C). Hyperthermia caused a considerable loss of cell viability that was accompanied by significant alterations in the tricarboxylic acid cycle, amino acids metabolism, urea cycle, glutamate metabolism, pentose phosphate pathway, and in the volatile signature associated with the lipid peroxidation process. Conclusion: These results provide novel insights into the mechanisms underlying hyperthermia-induced hepatocellular damage.

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Section: Introductionmentioning

confidence: 99%

Hepatic Metabolic Derangements Triggered by Hyperthermia: An In Vitro Metabolomic Study

et al. 2019

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“…Therapeutic hypothermia improves survival and neurodevelopmental outcomes in neonates with moderate to severe hypoxic ischaemic encephalopathy [11]. In adults, two phase-two trials comparing therapeutic hypothermia at 32-34 °C with a permissive approach to temperature management suggested that therapeutic hypothermia increased survival and improved neurological outcomes following out-of-hospital cardiac arrest [12, *Correspondence: paul.young@ccdhb.org.nz 1 Intensive Care Unit, Wellington Regional Hospital, Wellington, New Zealand Full author information is available at the end of the article 13]. A subsequent trial comparing two hypothermia regimens (33 and 36 °C) showed that these resulted in similar outcomes [14].…”

Section: Temperature Management In Patients With Hypoxic Brain Injuriesmentioning

confidence: 99%

“…]. As peripheral thermometry can substantially underestimate core body temperature [20] and temperature can rise rapidly [1], it is prudent to monitor core body temperature continuously in critically ill patients with fever. Although uncommon, there are certainly instances where patients develop extremely high body temperature (> 42 °C) and die soon after [6].…”

Section: Temperature Management In Patients With Traumatic Brain Injumentioning

confidence: 99%

“…In patients with hyperthermia, rather than fever, careful monitoring of body temperature and early intervention using physical cooling measures with or without neuromuscular paralysis is prudent. In this situation, impaired heat loss and/or excessive heat production can result in life-threatening complications such as rhabdomyolysis and secondary hyperkalemia, metabolic acidosis, multi-organ failure and disseminated intravascular coagulation [1].…”

Section: Severe Temperature Elevation and Hyperthermiamentioning

confidence: 99%

“…In patients with muscle rigidity and agitation, benzodiazepines can be used to reduce the generation of heat [1]. Although the use of bromocriptine and dantrolene has been reported in patients with neuroleptic malignant syndrome, and chlorpromazine and cyproheptadine can be used in serotonin syndrome, most patients with hyperthermia can be managed with supportive care and conventional cooling methods rather than requiring specific drug therapies [1]. One notable exception to this is in patients with malignant hyperthermia where dantrolene should be administered promptly [1].…”

Section: Severe Temperature Elevation and Hyperthermiamentioning

confidence: 99%

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When less is more in the active management of elevated body temperature of ICU patients

Young

Prescott

2019

Intensive Care Med

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Fever is a pathophysiological response in which the body's normal thermoregulatory set-point is adjusted upwards leading to an increase in body temperature. In contrast, hyperthermia occurs from excessive heat production or insufficient thermoregulation (e.g., heat stroke or drug reactions). Although temperature elevation is common in Intensive Care Unit (ICU) patients, a newly elevated body temperature should prompt consideration of a diagnostic evaluation. It is always prudent to consider the possibility of infection; however, for critically patients with acute brain pathologies in particular, elevated body temperature is common, even in the absence of infection. Body temperature may be elevated due to drugs, particularly antipsychotic, serotonergic, sympathomimetic, anesthetic, and anticholinergics drugs [1]. Thyrotoxicosis and pheochromocytoma should also be considered in the differential diagnosis. Often elevated temperature is multifactorial and, in many patients, particularly after major surgery, a specific cause is not found. Although body temperature is recorded assiduously in the ICU [2], it is often unclear when or how to intervene when a patient's body temperature is elevated. A recent individual patient data meta-analysis reported that more active fever management did not increase survival compared with less active fever management in an all-comers population of critically ill adults [3]. Survival by treatment group was similar in a range of subgroups defined by age, illness severity, receipt of specific organ supports, and the presence versus absence of high fever at baseline. These data suggest that, in general, when it comes to active management of fever in ICU patients, although less may not be more, doing less to treat fever results in similar outcomes to doing more.

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