A Case of Exertional Heat Stroke Complicated by Hypoxic Hepatitis.
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ABSTRACT:
SUBMITTER: Woitok BK
PROVIDER: S-EPMC7149357 | biostudies-literature | 2020
REPOSITORIES: biostudies-literature
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A Case of Exertional Heat Stroke Complicated by Hypoxic Hepatitis.
Woitok Bertram K BK Bahmad Shawki S Lindner Gregor G
Case reports in emergency medicine 20200330
<h4>Background</h4>Exertional heat stroke is a life-threatening condition often complicated by multiorgan failure. We hereby present a case of a 25-year-old male presenting with syncope after a 10 km run in 28°C outside temperature who developed acute liver failure. <i>Case Presentation</i>. Initial temperature was found to be 41.1°C, and cooling measures were rapidly applied. He suffered from acute renal failure and rhabdomyolysis and proceeded to acute liver failure (ASAT 6100 U/l and ALAT 65 ...[more]
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Project description:BackgroundThe aim of this study was to characterize the time-resolved progression of clinical laboratory disturbances days-following an exertional heat stroke (EHS). Currently, normalization of organ injury clinical biomarker values is the primary indicator of EHS recovery. However, an archetypical biochemical recovery profile following EHS has not been established.MethodsWe performed a retrospective analysis of EHS patient records in US military personnel from 2008-2014 using the Military Health System Data Repository (MDR). We focused on commonly reported clinical laboratory analytes measured on the day of injury and all proceeding follow-up visits.ResultsOver the prescribed period, there were 2,529 EHS episodes treated at 250 unique treatment locations. Laboratory results, including a standardized set of blood, serum and urine assays, were analyzed from 0-340 days following the initial injury. Indicators of acute kidney injury, including serum electrolyte disturbances and abnormal urinalysis findings, were most prevalent on the day of the injury but normalized within 24-48hours (creatinine, blood urea nitrogen, and blood and protein in urine). Muscle damage and liver function-associated markers peaked 0-4 days after injury and persisted outside their respective reference ranges for 2-16 days (alanine aminotransferase, aspartate aminotransferase, creatine phosphokinase, myoglobin, prothrombin time).ConclusionBiochemical recovery from EHS spans a 16-day time course, and markers of end-organ damage exhibit distinct patterns over this period. This analysis underscores the prognostic value of each clinical laboratory analyte and will assist in evaluating EHS patient presentation, injury severity and physiological recovery.
| S-EPMC7055888 | biostudies-literature
Project description:Exertional heat stroke (EHS) is a life-threatening medical condition involving thermoregulatory failure and is the most severe condition along a continuum of heat-related illnesses. Current EHS policy guidance principally advocates a thermoregulatory management approach, despite growing recognition that gastrointestinal (GI) microbial translocation contributes to disease pathophysiology. Contemporary research has focused to understand the relevance of GI barrier integrity and strategies to maintain it during periods of exertional-heat stress. GI barrier integrity can be assessed non-invasively using a variety of in vivo techniques, including active inert mixed-weight molecular probe recovery tests and passive biomarkers indicative of GI structural integrity loss or microbial translocation. Strenuous exercise is strongly characterised to disrupt GI barrier integrity, and aspects of this response correlate with the corresponding magnitude of thermal strain. The aetiology of GI barrier integrity loss following exertional-heat stress is poorly understood, though may directly relate to localised hyperthermia, splanchnic hypoperfusion-mediated ischemic injury, and neuroendocrine-immune alterations. Nutritional countermeasures to maintain GI barrier integrity following exertional-heat stress provide a promising approach to mitigate EHS. The focus of this review is to evaluate: (1) the GI paradigm of exertional heat stroke; (2) techniques to assess GI barrier integrity; (3) typical GI barrier integrity responses to exertional-heat stress; (4) the aetiology of GI barrier integrity loss following exertional-heat stress; and (5) nutritional countermeasures to maintain GI barrier integrity in response to exertional-heat stress.
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Project description:The frequency of exertional heat stroke (EHS) increases with the gradual elevation of global temperatures during summer. Acute kidney injury (AKI) is a common complication of EHS, and its occurrence often indicates the worsening of a patient's condition or a poor prognosis. In this study, a rat model of AKI caused by EHS was established, and the reliability of the model was evaluated by HE staining and biochemical assays. The expression of kidney tissue proteins in the EHS rats was analyzed using label-free liquid chromatography-tandem mass spectrometry. A total of 3,129 differentially expressed proteins (DEPs) were obtained, and 10 key proteins were finally identified, which included three upregulated proteins (Ahsg, Bpgm, and Litaf) and seven downregulated proteins (medium-chain acyl-CoA synthetase 2 (Acsm2), Hadha, Keg1, Sh3glb1, Eif3d, Ambp, and Ddah2). The qPCR technique was used to validate these 10 potential biomarkers in rat kidney and urine. In addition, Acsm2 and Ahsg were double-validated by Western blotting. Overall, this study identified 10 reliable biomarkers that may provide potential targets for the treatment of AKI caused by EHS.
| S-EPMC10291232 | biostudies-literature
Project description:To describe the possible association (pathophysiologic and clinical features) between exertional heat stroke (EHS) and malignant hyperthermia (MH).Both EHS and MH are acute and life-threatening disorders. It has repeatedly been shown that EHS can occur in well-trained patients with known MH-associated mutation in the RYR1 gene in the absence of any extreme environmental conditions or extreme physical activity, thereby supporting a possible link between EHS and MH. In this case, a highly trained 30-year-old male athlete suddenly collapsed while running. He had initial hyperthermia (40.2°C) and progressive multiple organ failure requiring medical management in an intensive care unit. After he recovered completely, a maximal exercise test was performed and showed an obvious abnormality of oxidative metabolism in muscle; genetic analysis of the RYR1 gene identified a heterozygous missense variation p.K1393R. Consequently, the athlete was given appropriate information and allowed to progressively return to sport competition.Doping, use of drugs and toxic agents, exercise-associated hyponatremia, exertional heat illness.Initial management started with the basic resuscitative guidelines of airway, breathing, and circulation (intubation). Cooling, administration of fresh frozen plasma, and intensive rehydration resulted in improvement.To our knowledge, ours is the first description of this MH mutation (p.K1393R) in the RYR1 gene that was associated with exertional rhabdomyolysis involving a dramatic impairment of oxidative metabolism in muscle.Common features are shared by EHS and MH. Careful attention must therefore be paid to athletes who experience EHS, especially in temperate climates or when there are no other predisposing factors.
| S-EPMC4732402 | biostudies-literature
Project description:Exertional heat stroke (EHS) is a life-threatening illness and leads to multi-organ dysfunction including acute kidney injury (AKI). The clinical significance of abnormal electrolytes and renal outcomes in ESH patients has been poorly documented. We aim to exhibit the electrolyte abnormalities, renal outcomes and risk factors of patients with AKI receiving dialysis in EHS.A retrospective cohort study in EHS patients between 2003 and 2014 were conducted. Clinical and laboratory outcomes including serum and urine electrolytes, AKI and dialysis were assessed on admission, during hospitalization and at the time of their discharge from the hospital. A logistic regression analysis was performed for risk factors of acute dialysis.All 66 subjects with mean age 22.1?±?4.3 years were included. On admission, the common electrolyte disturbances were hypokalemia (71.2 %), hypophosphatemia (59.1 %), hyponatremia (53.0 %), hypocalcemia (51.5 %), and hypomagnesemia (34.9 %). Electrolytes depletion was confirmed as renal loss (potassium loss; 54.2 %, phosphate loss; 86.7 %, sodium loss; 64.7 % and magnesium loss; 83.3 %). During hospitalization ranging from 2 to 209 days, 90.9 % patients suffered from AKI with 16.7 % receiving acute dialysis, and 3 % patients died. At discharge, AKI and electrolyte abnormalities had dramatically improved. The prognosis factors for AKI receiving dialysis were identified as neurological status, renal function and serum muscle enzyme at time of admission.The study suggests that hypoelectrolytemia and AKI are frequently observed in patients with EHS. Neurological impairment, impaired renal function, and increased serum muscle enzyme should be considered risk factors of acute dialysis.
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Project description:Increased gut permeability is implicated in the initiation and extent of the cytokine inflammatory response associated with exertional heat stroke (EHS). The primary objective of this study was to determine if a five amino acid oral rehydration solution (5AAS), specifically designed for the protection of the gastrointestinal lining, would prolong time to EHS, maintain gut function and dampen the systemic inflammatory response (SIR) measured during EHS recovery. Male C57/BL6J mice instrumented with radiotelemetry were gavaged with 150 μL of 5AAS or H2 O, and ≈12 h later were either exposed to an EHS protocol where mice exercised in a 37.5°C environmental chamber to a self-limiting maximum core temperature (Tc,max) or performed the exercise control (EXC) protocol (25°C). 5AAS pretreatment attenuated hypothermia depth and length (p < 0.005), which are indicators of EHS severity during recovery, without any effect on physical performance or thermoregulatory responses in the heat as determined by percent body weight lost (≈9%), max speed (≈6 m/min), distance (≈700 m), time to Tc,max (≈160 min), thermal area (≈550°C∙min), and Tc,max (42.2°C). EHS groups treated with 5AAS showed a significant decrease in gut transepithelial conductance, decreased paracellular permeability, increased villus height, increased electrolyte absorption and changes in tight junction protein expression pattern suggestive of improved barrier integrity (p < 0.05). No differences were witnessed between EHS groups in acute phase response markers of liver, circulating SIR markers, or indicators of organ damage during recovery. These results suggest that a 5AAS improves Tc regulation during EHS recovery through maintaining mucosal function and integrity.
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Project description:Exertional heat stroke (EHS) is a life-threatening disease characterized by high mortality and incidence of rhabdomyolysis (RM). It would therefore be valuable to establish a stable EHS-induced RM model that accurately reflects the clinical characteristics of EHS patients and provides an objective animal model for further study of the pathogenesis of RM. In the current study, 8∼9-week-old, male, wild-type C57BL/6J mice, at the stage of sexual maturity, were randomly divided into four groups: the EHS group, the classical heat stroke (CHS) group, the sham heat exercise group, and sham heat rest group. The survival rate of mice was determined under relatively high levels of temperature and humidity (37.5°C, 65% relative humidity (RH); 37.5°C, 70% RH; 39.5°C, 65% RH; and 39.5°C, 70% RH) as well as a high core temperature (Tc; 42, 42.5, and 43°C). Results showed that the environmental condition of 39.5°C and 65% RH was most suitable for EHS modeling. The end point of EHS evaluation was exhaustion or an individual's core temperature reaching 43°C. The survival rate of mice in the EHS group within 24 h under these conditions was 37.34%, which is consistent with the high mortality characteristics noted in EHS patients. Severe RM was observed in the EHS group by H&E staining and transmission electron microscopy. Creatine kinase levels in the EHS group mostly exceeded 10,000 U/L, which was approximately 10 times higher than that in the sham heat rest group. Renal tubules of the EHS group exhibited severe necrosis, and calcium overload in the skeletal muscles of this group was also observed using intravital 2-photon microscopy. In conclusion, we made improvements to a stable EHS-induced RM animal model to truly reflect the clinical characteristics of EHS patients. This new model should be helpful in the further study of RM pathogenesis.
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Project description:BackgroundAmphetamine use causes cardiomyopathy via catecholamine-mediated effects such as tachycardia, hypertension, vasoconstriction, and direct cardio-toxic effects. Traditionally, an increased risk of haemorrhagic stroke is associated with amphetamine use. However, up to one-third of stimulant-associated cardiomyopathy patients have left ventricular (LV) thrombus formation leading to an increased risk of systemic embolization. We report a case of amphetamine-induced cardiomyopathy complicated by embolic stroke secondary to LV thrombus.Case summaryA 38-year-old man with 6-month history of sustained amphetamine use presented to the emergency department with left-sided weakness, facial droop, and dysarthria. Angiography confirmed right middle cerebral artery thrombus. Prompt mechanical thrombectomy yielded full neurological recovery. Dyspnoea prompted transthoracic echocardiography showing dilated cardiomyopathy with an ejection fraction of 5% and LV thrombus. Anticoagulation was initiated with warfarin as well as pharmacological therapy for heart failure with reduced ejection fraction including bisoprolol, spironolactone, loop diuretic, and sacubitril/valsartan. He was discharged successfully following resolution of ventricular thrombus and medical management of heart failure. Clinical recovery was hampered by psychosocial factors resulting in non-adherence to medical therapy and continued amphetamine use.ConclusionSustained amphetamine use can result in severe dilated cardiomyopathy with LV thrombus formation and embolic complications such as ischaemic stroke. Avoidance of amphetamines in conjunction with guideline-directed pharmacological management are key components of therapy. However, psychosocial factors can exert significant influence on recovery.
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Project description:Diabetic striatopathy (DS) is a rare complication secondary to hyperglycemia, featured by the choreiform movements and reversible striatal abnormalities on neuroimaging. Several studies have described the clinical characteristics of DS, however, the simultaneous occurrence of DS and acute ischemic stroke (AIS) in the striatum has not been reported. Herein, we report a 68-year-old man with uncontrolled type 2 diabetes who experienced the progressive involuntary movement of the right upper and lower limbs for 10 days. We initially considered this patient as an AIS with hemorrhage in the left basal ganglia and adjacent area because his brain magnetic resonance imaging (MRI) showed hyperintensity on fluid-attenuated inversion recovery (FLAIR) and diffusion-weighted imaging (DWI) images, as well as slight T1-hyperintensity around T1-hypointensity. However, his symptoms worsen persistently, which was inconsistent with neuroimaging findings. Further computed tomography (CT) scan revealed an extensive hyper-density and focal low-density in the left striatum, suggesting the diagnosis of DS and AIS. His symptoms were in complete remission after 2 months of glucose control. However, striatal hyperintensity on T1 images was significantly increased compared to the initial images, which disappeared 18 months later. Additionally, DWI hyperintensity on infarction lesions disappeared, while softening lesions and gliosis were observed on the follow-up MRI images. Therefore, we finally diagnosed the patient as DS complicated with AIS. This report highlights that DS and AIS could occur simultaneously in the striatum after hyperglycemia, which is easily misdiagnosed as AIS with hemorrhage and requires clinicians to pay more attention to avoid misdiagnosis and delayed treatment.
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Project description:Only a few authors have reported about a new-onset headache among patients who sustained an episode of an exertional heat illness (EHI). This report presents a healthy and physically fit 20-year-old male who developed a completely new headache after an EHI event. The new headache could be aggravated or called by exertion or exposure to sun and environmental heat. It was severe enough to interfere with even moderate physical activity, but reacted well to a few hours' rest and OTC pain medications. An extensive work-up including laboratory blood tests, lumbar puncture, head CT, and CT angiogram was negative. The patient remained symptomatic on the 6-month follow-up. Continued abstinence from physical activity and waiting for spontaneous resolution were recommended. We suggest that the headache may be secondary to the hyperthermia brain damage during the EHI event and differs from exertional headache by its association with exposure to sun and environmental heat.
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