Heat stroke with sepsis: A case report and review of the literature

Abstract

Heat stroke, triggered by excessive heat exposure or intense physical activity, is a medical condition characterized by a rapid rise in core body temperature, central nervous system dysfunction and multiorgan failure. A patient presented with heat stroke and was unconscious. During treatment, we identified a range of complications, including shifted flora, coagulation abnormalities, liver damage and renal failure—indicating multiorgan dysfunction. We administered antibiotic therapy, blood purification and other comprehensive treatments, leading to the patient’s recovery and subsequent discharge. For cases of heat stroke in an intensive care setting, clinicians must recognize the condition early and act swiftly to reduce body temperature. Additionally, the early use of antibiotics can help prevent microbial imbalance. For eligible patients, hemodialysis should be initiated promptly to manage renal complications effectively.

Introduction

Heat stroke (HS) is a life-threatening condition affecting the central nervous system and leading to multiorgan dysfunction caused by body temperatures above 40°C.1 In HS, the disruption of thermoregulatory mechanisms results in hyperthermia, hemodynamic impairment, organ dysfunction and potentially death. Activated coagulation and inflammation play critical roles in the microcirculatory impairment of HS, alongside dehydration and energy imbalances.^1,2 According to The Lancet’s analysis of extreme weather and mortality, globally, approximately 365,000 people died as a result of extreme heat in 2019 alone. ³ Because of climate change, HS-related deaths are projected to increase by nearly 2.5 times by 2050. ⁴

According to its etiology, there are two types of HS: classical HS and exertional HS. ⁵ The progression from less severe heat-related illnesses to HS (the most severe form of heat-related illness) depends on various factors, including environmental conditions, age, medications and comorbidities. The mortality rate for HS patients ranges between 30% and 60%, even with intensive care. Survivors may also experience long-term neurologic and cardiovascular complications.^6,7 Therefore, in cases of HS, the primary treatment measure is rapid, effective and sustained cooling, which significantly reduces patient mortality and facilitates subsequent treatments.

Elucidating the pathophysiologic changes and mechanisms underlying HS has been a central focus of heat-related illness research, recently leading to numerous advances in our knowledge and understanding of this condition. In HS, the integrity of the gastrointestinal tract is compromised, allowing endotoxins and pathogens to enter the circulation, triggering endotoxemia. ⁸ Overheating can denature proteins, phospholipids and lipoproteins, as well as liquefy membrane lipids, which may result in cardiovascular failure, multiorgan dysfunction and, ultimately, death. ¹

We present the case of a man in his early 80s who developed multiple organ failure following pyrexia. Throughout his treatment period, which included anti-infective therapy, continuous mechanical ventilation and blood purification, we observed significant shifts in the patient’s microbial flora. Following a comprehensive therapeutic regimen, the patient recovered and was discharged from the hospital.

Case report

A man in his early 80s was admitted to the emergency department of Shandong Third Hospital (affiliated with Shandong University) for unconsciousness on a hot night (5 August 2024). HS was suspected because of high fever, disturbance of consciousness and the patient resting in a poorly ventilated room without any cooling measures. Upon physical examination, body temperature was 41°C, blood pressure was 112/70 mmHg, pulse rate was 112 beats/min and respiratory rate was 29 breaths/min, and the patient was in a coma. A small amount of wet rhonchi could be heard in the lungs, and a neurologic examination showed that the tendon reflexes had disappeared. Bilateral pathologic signs (+) and assessment of other systems revealed no other abnormalities. The patient had no history of infection or antibiotic use before the condition’s onset.

Laboratory investigations showed a white blood cell (WBC) count of 13.16 × 10⁹/L with 90.6% neutrophils and 5.6% lymphocytes, a platelet count of 165 × 10⁹/L, erythrocytes of 5.02 × 10¹²/L, hemoglobin of 15.9 g/L, serum myoglobin of 1303 ng/mL, plasminogen time of 16.40 s, activated partial plasminogen time of 86.30 s, urea 10.7 mmol/L, creatinine 110.7 μmol/L, alanine aminotransferase 177.4 U/L; aspartate aminotransferase 244.3 U/L, procalcitoninogen 2.5 ng/mL, pH 7.48, PaCO₂ 27 mmHg, PO₂ 100 mmHg (fraction of inspired oxygen [FiO₂], 41%) and lactic acid 1.8 mol/L. Cranial computed tomography (CT) scan at admission showed no obvious cerebrovascular disease such as hemorrhage or infarction; chest CT scan showed signs of bronchitis; urinalysis showed a reddish-brown urine color.

The patient was diagnosed with pyrexia, acute renal and hepatic failures, rhabdomyolysis and coagulation abnormalities. Upon admission to the hospital, the patient presented with shortness of breath, a respiratory rate of 33 breaths/min and oxygen saturation (SpO₂) of 88%. Given the presence of respiratory failure, endotracheal intubation was performed, and the patient was placed on ventilator-assisted respiration in pressure support ventilation mode, with positive end-expiratory pressure of 8 mmHg and a FiO₂ of 45%. Analgesia and sedation were administered, along with other supportive treatments. Furthermore, the patient exhibited abnormal coagulation function and was given suspended red blood cells to address this issue. Because of elevated creatinine levels and metabolic acidosis, continuous blood purification (CBP) therapy was initiated using continuous venovenous hemofiltration with dialysis (CVVHDF) at a blood flow rate of 150 mL/min. Additional treatment measures included rehydration, cooling, nutritional support, sodium bicarbonate administration and other comprehensive supportive therapies. The patient’s family provided written informed consent to treatment because the patient remained in a coma.

Overall, these initial assessments showed that the patient was admitted to the hospital with a high fever, elevated infection markers and a chest CT scan indicating bronchitis. Consequently, blood cultures, sputum cultures and respiratory pathogen microbiologic tests were conducted. The patient was initially treated with empirical antibiotics (cefoperazone–sulbactam, 4.5 g) intravenously, every 8 hours. The blood cultures revealed Staphylococcus aureus, the sputum cultures identified Citrobacter krebsiensis and the respiratory pathogen microbiologic examination detected Acinetobacter baumannii and Escherichia coli. Following treatment with cefoperazone–sulbactam, the patient’s infection indicators decreased (WBC count: 8.36 × 10⁹/L). The antibiotic regimen was modified based on drug-sensitivity tests. To monitor the efficacy of the antibiotics, we examined the patient’s chest CT scans at regular intervals from admission to discharge (Figure 1).

Figure 1.

Patient computed tomography (CT) scans during hospitalization: (a) CT images on the day of admission; (b) CT images 3 days after admission and (c) CT images before discharge.

The changes in chest CT scans indicated that the cefoperazone–sulbactam treatment had some efficacy. Three days after admission, the patient’s oxygen saturation reached 99% and the respiratory rate was normal. Consequently, the medical team removed the tracheal tube to facilitate respiratory therapy. By the fourth day of hospitalization, multiple coagulation function assessment and creatinine levels indicated a gradual improvement. Therefore, the medical team opted to discontinue the CBP treatment. The patient continued to receive anti-infective therapy, enteral nutrition and other supportive treatments throughout this period. Following the prescribed interventions, the patient was discharged 11 days after admission. At discharge, the patient expressed satisfaction with the treatment received and reported feeling much better. He also expressed appreciation for the timely and thorough care provided.

The reporting of this study conforms to the Case Report (CARE) guidelines, ⁹ and all patient details were de-identified. The study was not submitted to an ethics review committee for approval, as it is a retrospective case report that involved collecting anonymized data without interventions beyond standard medical care. The patient provided verbal informed consent to publish the case report and accompanying images.

Discussion

A range of acute syndromes comprise HS. Following its onset, HS can manifest through two primary mechanisms. The first involves direct damage to organs and systems caused by an elevation in core temperature resulting from heat exposure. The second involves heat stress and endotoxemia due to heat exposure, which can trigger a systemic inflammatory response and immune dysfunction. This pathologic process is referred to as a sepsis-like reaction to pyrexia, leading to multiorgan dysfunction in the patient.^10,11

In the present case, the first key point we need to focus on is flora displacement. The intestinal tract is the largest reservoir of bacteria and endotoxins in the body, and its unique physiologic environment is an important factor in the pathophysiologic processes involved in systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS).^12,13 The intestinal mucosal barrier has a complex composition, dominated by the surface mucus layer, the epithelial cell layer and the mucosal basal layer, with mechanical, chemical, immune and biological barriers. The functional ability of the intestinal mucosa barrier is affected by various factors. When the intestinal barrier is degraded, intestinal bacteria migrate into the body. Bacteria, endotoxin and antibody mediators entering the circulation induce the release of inflammatory mediators, which triggers and exacerbates uncontrolled SIRS and bacterial translocation in the form of endotoxemia or bacteremia. Simultaneously, SIRS further aggravates intestinal barrier function, forming a vicious cycle, ultimately leading to MODS. Gastrointestinal lesions (such as damage to the intestinal mucosa), apoptosis of intestinal epithelial cells and increased intestinal permeability can occur in severe HS.^14–17 Furthermore, previous studies suggested that bacterial translocation may also be involved in the pathophysiologic process of HS. ¹⁸ In short, HS impairs the function of the gastrointestinal tract by damaging the small intestine and slowing the rate of emptying of the gastrointestinal tract. It also disrupts the tight junctions of the gastrointestinal tract cells, resulting in barrier dysfunction and bacteria leaking into the circulation.^19,20 In this case, the patient’s blood cultures showed human Staphylococcus after HS, sputum cultures showed Citrobacter graminearum and respiratory pathogenic microbiologic examination showed E. coli and A. baumannii. Concurrently, the patient’s infection indicators, such as procalcitonin and WBC count gradually rose, and chest CT scan showed extensive patchy pneumonia. After receiving antibiotic treatment, the patient’s indicators stabilized, no obvious bacterial growth was seen on repeated cultures and the extensive patchy pneumonia seen on chest CT scan gradually dissipated. This case shows us that antibiotic treatment is necessary for patients with HS, simultaneously with enteral nutrition therapy for patients in coma, and intestinal management needs careful consideration.

Treating patients with severe HS requires early and standardized CBP, which is not purely renal replacement and needs to be applied continuously depending on the progress of the condition.^21,22 Treatment with CBP is an important means of implementing intravascular hypothermia, which can manage the patient’s body temperature, ²³ remove inflammatory mediators, play an anti-inflammatory role, remove myoglobin, bilirubin and other harmful substances,^22,24 and effectively control fluid volume while protecting the patient’s renal function. ²⁵ Previously, Wakino et al. ²⁶ also reported a case of cold hemodialysis combined with continuous cold hemodiafiltration, successfully treating a case of HS with multiple organ failure, which also indicates that CBP and other treatments should be initiated early. Recent studies have demonstrated that CVVHDF with HA380 HP therapy can significantly improve organ function in patients with pyrexia and MODS, effectively improve the recovery rate and reduce the morbidity and mortality of patients with severe pyrexia. ²⁷ In the present case, the patient received prompt hemodialysis upon admission. However, their coagulation function was abnormal at admission, which led to the decision not to proceed with continuous renal replacement therapy. This scenario highlights the need for further research into the optimal timing and frequency of continuous renal replacement therapy for treating multiorgan failure.

Finally, injuries occurring within the “golden 30 minutes” following the pyrexia onset can be addressed by reducing core body temperature below 39°C, which can achieve a mortality rate of zero and rarely leaves any lasting sequelae. ²⁸ Rapid cooling measures are critical to the successful treatment outcomes, restricting time to develop long-term organ damage and buying time for resuscitation. Most cases of HS can be prevented with appropriate strategies to mitigate heat stress. In environments with high heat and humidity, high-risk groups need to seek methods to lower indoor temperatures, reduce outdoor exercise at the hottest times of day and be aware of the first aid treatment of HS, which can significantly reduce HS incidence.

Conclusion

The most severe heat-related illness is HS. Given its high mortality rate, early recognition and prompt treatment to lower body temperature in an intensive care setting offer the best chance of survival with minimal long-term complications. The treatment should focus on preventing microbial imbalance, and hemodialysis should be initiated as early as possible for patients experiencing multiple organ failure.