A Case of Severe Heatstroke and Review of Pathophysiology, Clinical Presentation, and Treatment

Horseman, Michael A.; Rather-Conally, Jacquelyn; Saavedra, Crystal; Surani, Salim

doi:10.1177/0885066611434000

Cited by 11 publications

(17 citation statements)

References 34 publications

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“…Endotoxemia has been reported to at least partially contribute to the inflammatory manifestations of several heterogeneous pathologies including heat stroke, inflammatory bowel disease and other autoimmune disorders, severe pancreatitis, ethanol-induced liver disease, HIV infection, insulin resistance, obesity, diabetes mellitus, chronic heart failure, atherosclerosis, memory impairment, multiple trauma, hemorrhagic shock, burns, chronic kidney disease, and asthma exacerbation [26, 31, 39-53]. Circulating levels have also been found in patients with a ruptured abdominal aortic aneurysm [54].…”

Section: Introductionmentioning

confidence: 99%

Endotoxin, Toll-like Receptor-4, and Atherosclerotic Heart Disease

Bowman

Surani

Horseman

2017

CCR

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Background:Endotoxin is a lipopolysaccharide (LPS) constituent of the outer membrane of most gram negative bacteria. Ubiquitous in the environment, it has been implicated as a cause or con-tributing factor in several disparate disorders from sepsis to heatstroke and Type II diabetes mellitus. Starting at birth, the innate immune system develops cellular defense mechanisms against environmen-tal microbes that are in part modulated through a series of receptors known as toll-like receptors. Endo-toxin, often referred to as LPS, binds to toll-like receptor 4 (TLR4)/ myeloid differentiation protein 2 (MD2) complexes on various tissues including cells of the innate immune system, smooth muscle and endothelial cells of blood vessels including coronary arteries, and adipose tissue. Entry of LPS into the systemic circulation ultimately leads to intracellular transcription of several inflammatory mediators. The subsequent inflammation has been implicated in the development and progression atherosclerosis and subsequent coronary artery disease and heart failure.Objective:The potential roles of endotoxin and TLR4 are reviewed regarding their role in the pathogen-esis of atherosclerotic heart disease.Conclusion:Atherosclerosis is initiated by inflammation in arterial endothelial and subendothelial cells, and inflammatory processes are implicated in its progression to clinical heart disease. Endotoxin and TLR4 play a central role in the inflammatory process, and represent potential targets for therapeutic intervention. Therapy with HMG-CoA inhibitors may reduce the expression of TLR4 on monocytes. Other therapeutic interventions targeting TLR4 expression or function may prove beneficial in athero-sclerotic disease prevention and treatment.

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Section: Introductionmentioning

confidence: 99%

Endotoxin, Toll-like Receptor-4, and Atherosclerotic Heart Disease

Bowman

Surani

Horseman

2017

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“…15 Aunque no se pudo demostrar una causa infecciosa, es altamente probable que las alteraciones clínicas de la paciente fueran consecuencia de la hipertermia, ya que no se observaron signos indirectos de inflamación, como ascenso de los niveles de proteína C reactiva. Además, la magnitud de la elevación de las enzimas musculares y hepá-ticas no es frecuente de observar en los episodios de shock séptico.…”

Section: Discussionunclassified

Falla multiorgánica asociada a hipertermia en una lactante con síndrome de Prader-Willi. Caso clínico

Donoso¹,

Arriagada²,

Campbell³

et al. 2013

Arch Argent Pediat

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RESUMENEl golpe de calor es una emergencia médica y se debe entender como una forma de hipertermia asociada a una respuesta inflamatoria sistémica, que ocasiona falla multiorgánica y en la cual la disfunción del sistema nervioso central es predominante. Si no es tratada precozmente, puede ocasionar una alta mortalidad. El síndrome de Prader-Willi es un trastorno genético multisistémico secundario a una anormalidad en el brazo largo del cromosoma 15 (15q11-q13), caracterizado por hipotonía central neonatal, retraso del desarrollo psicomotor, hipogonadismo, hiperfagia y obesidad. Estos pacientes son proclives a presentar problemas de termorregulación. Se comunica el caso de una lactante de 5 meses en quien se estableció el diagnóstico de síndrome de Prader-Willi en el curso de un episodio febril sin foco conocido, que evolucionó con falla multiorgánica y rabdomiólisis secundaria a la hipertermia. Palabras clave: síndrome de Prader-Willi, hipertermia, golpe de calor, falla multiorgánica. AbStRActHeat stroke is a medical emergency characterized primarily by an elevated core temperature associated with a systemic inflammatory response, which causes multiple organ dysfunction in which encephalopathy predominates. If it is not early treated has high mortality. The Prader-Willi syndrome is a multisystem genetic disorder secondary to an abnormality in long arm chromosome 15 (15q11-q13), characterized by neonatal central hypotonia, developmental delay, hypogonadism, hyperphagia and obesity. These patients are susceptible to developing thermoregulatory problems. We report the case of a 5-month-old infant, in whom a diagnosis of Prader-Willi syndrome was established in the course of a febrile episode without known focus, who developed multiorganic failure and rhabdomyolysis secondary to hyperthermia.

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“…The pathogenesis of heat stress and strain has been examined within sports medicine, emergency medicine, ecological studies, and occupational health [3,5,[49][50][51][52][53][54][55][56][57][58][59][60][61][62][63]. Among this diversity, there is remarkable consensus on precipitating biological factors that correlate heat stress and fatal heat stroke.…”

Section: Heat Stroke and Elevation Of Intestinal Permeabilitymentioning

confidence: 99%

Enhanced intestinal permeability and intestinal co-morbidities in heat strain: A review and case for autodigestion

et al. 2021

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Enhanced intestinal permeability is a pervasive issue in modern medicine, with implications demonstrably associated with significant health consequences such as sepsis, multiorgan failure, and death. Key issues involve the trigger mechanisms that could compromise intestinal integrity and increase local permeability allowing the passage of larger, potentially dangerous molecules. Heat stress, whether exertional or environmental, may modulate intestinal permeability and begs interesting questions in the context of global climate change, increasing population vulnerabilities, and public health. Emerging evidence indicates that intestinal leakage of digestive enzymes and associated cell dysfunctions--a process referred to as autodigestion--may play a critical role in systemic physiological damage within the body. This increased permeability is exacerbated in the presence of elevated core temperatures. We employed Latent Dirichlet Allocation (LDA) topic modeling methods to analyze the relationship between heat stress and the nascent theory of autodigestion in a systematic, quantifiable, and unbiased manner. From a corpus of 11,233 scientific articles across four relevant scientific journals (Gut, Shock, Temperature, Gastroenterology), it was found that over 1,000 documents expressed a relationship between intestine, enhanced permeability, core temperature, and heat stress. The association has grown stronger in recent years, as heat stress and potential autodigestion are investigated in tandem, yet still by a limited number of specific research studies. Such findings justify the design of future studies to critically test novel interventions against digestive enzymes permeating the intestinal tract, especially the small intestine.

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A Case of Severe Heatstroke and Review of Pathophysiology, Clinical Presentation, and Treatment

Cited by 11 publications

References 34 publications

Endotoxin, Toll-like Receptor-4, and Atherosclerotic Heart Disease

Endotoxin, Toll-like Receptor-4, and Atherosclerotic Heart Disease

Falla multiorgánica asociada a hipertermia en una lactante con síndrome de Prader-Willi. Caso clínico

Enhanced intestinal permeability and intestinal co-morbidities in heat strain: A review and case for autodigestion

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