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cover of episode Ep 140: A 45-Year-Old Man with Confusion After Running

Ep 140: A 45-Year-Old Man with Confusion After Running

2025/4/3
logo of podcast Harrison's PodClass: Internal Medicine Cases and Board Prep

Harrison's PodClass: Internal Medicine Cases and Board Prep

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Dr. Charlie Wiener
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Dr. Kathy Handy
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Dr. Kathy Handy: 我主要关注的是患者病情的严重程度以及潜在的并发症。患者体温极高,意识状态改变,这提示可能存在严重的热射病。我们需要全面评估患者的病史,以排除败血症或药物中毒等其他可能性。此外,我还详细阐述了人体体温调节的生理机制,包括蒸发、辐射、传导和对流四种散热方式,以及影响汗液蒸发的因素,例如出汗过多、衣物过紧、湿度过高和脱水。在讨论中,我强调了热射病的临床分型(经典型和劳力型),以及不同类型热射病的临床表现和治疗方法。最后,我总结了热射病的诊断标准、潜在的并发症(如急性肾衰竭、心肌病、DIC和肝衰竭)以及治疗策略(快速降温、支持治疗和多器官衰竭的处理)。 Dr. Charlie Wiener: 我主要负责介绍病例,并参与讨论诊断和治疗方案。我首先描述了45岁健康男性在高温环境下长跑后出现意识混乱,体温高达42.5摄氏度,血压、心率、呼吸频率等指标异常的病例。在讨论中,我补充了关于热射病病理生理机制的细节,包括人体散热机制以及影响汗液蒸发的因素。我参与了对患者病情严重程度的评估,并提出了热射病的诊断和鉴别诊断,包括与败血症和药物中毒的鉴别。此外,我还详细解释了经典型和劳力型热射病的区别,并对热射病的潜在并发症(如急性肾衰竭、心肌病、DIC和肝衰竭)进行了讨论。最后,我参与了治疗方案的讨论,包括快速降温方法(蒸发降温、冷敷等)以及对急性肝衰竭患者的肝移植治疗方案。

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This is Katarina Heidhausen, Executive Editor of Harrison's Principles of Internal Medicine. Harrison's Pod Class is brought to you by McGraw-Hills Access Medicine, the online medical resource that delivers the latest content from the best minds in medicine. And now, on to the episode. Hi, everyone. Welcome back to Harrison's Pod Class. We're your co-hosts. I'm Dr. Kathy Handy. And I'm Dr. Charlie Wiener, and we're joining you from the Johns Hopkins School of Medicine.

Welcome to episode 140, a 45-year-old's man with confusion after running. Kathy, today I'm dragging you back to the ICU. All right, tell us about the case today. Today's patient is a 45-year-old man who's in great health and takes no medication. He is a frequent runner. On a hot August day, he goes out for his typical seven-mile run. About two hours later, he's found outside his house confused and unable to stand.

EMS is called and he's found to have a core temperature of 42.5 degrees centigrade with a blood pressure of 100 over 70, heart rate of 110, respiratory rate of 30, and an oxygen saturation of 98%. He's confused and is brought to the hospital and admitted directly to the ICU.

Wow, that's a temperature over 106 degrees Fahrenheit. So, sounds like we should at least talk about heat-related illness, but we need to get a full history to make sure this is not sepsis or drug intoxication is another consideration. Okay, so more history. His partner says he's been in great health and has no history of any drug or alcohol use. That morning was typical for him and a seven-mile run is routine.

As I mentioned, it was a typical hot August summer day in the southeast with temperatures in the 80s and a high humidity. Okay, so let's focus on heat-related illness. Let me start with some pathophysiology of heat regulation.

Strenuous exercise, as in our patient, can increase heat generation up to 20-fold. The heat load from metabolic heat production and environmental heat absorption is balanced by a variety of heat dissipation mechanisms. Normally, the body dissipates heat into the environment via four mechanisms. First is evaporation of skin moisture, and that's the single most efficient mechanism of heat loss, but it becomes progressively ineffective as the relative humidity rises to over 70%.

Second is radiation of infrared electromagnetic energy directly into the surrounding environment, which occurs continuously. Third is conduction, or the direct transfer of heat to a cooler object. And lastly, there is convection, the loss of heat to air currents, which becomes ineffective when the environmental temperature exceeds the skin temperature. Okay, sweating is the most important, which I assume requires proper hydration.

Right. Plus, we need to be cognizant of factors that interfere with the evaporation of sweat as they will significantly increase the risk of heat illness. Examples of this include dripping of sweat off the skin, constrictive or occlusive clothing, excessive humidity, and as you said, any pre-existing volume depletion. Okay. So back to our patient. He has a very high temperature and altered mental status. How would you characterize his disorder?

Heat-related illnesses do exist on a spectrum from less catastrophic like heat cramps through heat exhaustion and at the other extreme heat stroke. Tell me about heat stroke.

The clinical manifestations of heat stroke reflect a total loss of thermoregulatory function. Typical vital sign abnormalities include tachypnea, tachycardia, relative or absolute hypotension, and a widened pulse pressure. Although there is no single specific diagnostic test, the historical and physical triad of exposure to a heat stress, CNS dysfunction, and a core temperature over 40.5 degrees Celsius helps establish the preliminary diagnosis.

And there are two clinical forms of heat stroke, classical heat stroke and exertional heat stroke. I'm assuming based on the history that our patient has the exertional form, but what's the difference? Classic heat stroke usually occurs during long periods of high ambient temperature and humidity, as during summer heat waves. Patients commonly have chronic diseases that predispose to heat-related illness, and they may have limited access to oral fluids or cooling, such as air conditioning.

Patients with classic heat stroke are taking medications that can impair tolerance to a heat stress. The elderly are particularly at risk. Clinically, these patients are dehydrated, sweating has ceased, and the skin is hot and dry. Tell me a little bit more about exertional heat stroke then.

Patients with exertional heat stroke, in contrast to those with classic heat stroke, are often young and previously healthy, and their diagnosis is usually more obvious from the history. Athletes, laborers, and military recruits are common victims. Unlike those with classic heat stroke, many with exertional heat stroke present profusely diaphoretic despite significant dehydration. Okay, well it sounds like our patient has exertional heat stroke, which brings me to the question.

All of the following clinical manifestations of heat stroke are likely in this patient except A, acute renal failure, B, cardiomyopathy, C, disseminated intravascular coagulation or DIC, D, fulminant liver failure, or E, hypercalcemia. Okay, well, your question is really highlighting the severity of heat stroke. So the answer is E.

Patients with heat stroke, particularly exertional heat stroke, often have rhabdomyolysis with hypocalcemia and hyperphosphatemia. And the hypocalcemia may be symptomatic, so should be monitored closely. Okay, so hypercalcemia is the wrong answer, but let's run through the others so we have a more full picture of our patient's potential clinical course.

Well, first, renal failure can occur via a variety of mechanisms, including the volume depletion, the rhabdo, and even direct thermal injury. What about the cardiomyopathy? Patients with either form of heat stroke can have a thermal cardiomyopathy. They will have increases in cardiac biomarker levels and can have signs of heart failure despite their volume depletion. The ECG commonly displays a variety of tachyarrhythmias, nonspecific STDT wave changes, and even heat-related ischemia or infarction.

Our question tells us that patients may even have DIC and fulminant hepatic failure.

Yes, above about 42 degrees Celsius, heat can rapidly produce direct cellular injury. Thermosensitive enzymes become non-functional, and eventually there's irreversible uncoupling of oxidative phosphorylation. The production of heat shock proteins increases, and cytokines mediate a systemic inflammatory response. The vascular endothelium is also damaged, and this injury activates the coagulation cascade.

Significant shunting away from the splanchnic circulation produces gastrointestinal ischemia. Endotoxins further impair normal thermoregulation. As a result, severe hepatic dysfunction, permanent renal failure, disseminated intravascular coagulation, and fulminant multisystem organ failure can occur. Wow. Let's discuss treatment. How do you treat this gentleman?

Rapid cooling is the key to managing heat stroke and there are a variety of mechanisms to achieve that. But remember, peripheral measurements of temperature will not be accurate. You do need to monitor central or core temperatures. Evaporative cooling is frequently the most practical and effective technique. Cool water can be sprayed on the exposed skin while fans direct continuous airflow over the moistened skin.

Cold packs applied to the neck, axilla, and groin are useful cooling adjuncts. And there are also a variety of ICU cooling tools that are used for post-resuscitation cooling that may be employed. Immersion in cold water is generally not advisable because it may cause peripheral vasoconstriction and shivering, which delays central cooling.

And in cases of fulminant hepatic failure, I know that liver transplants have even been performed. And what's interesting is that in the liver explant, they see extensive pathologic findings consistent with hepatocyte death due to heat shock. Yes. And some patients, you know, in that scenario could get liver transplant and still go on to have really excellent outcomes.

Okay, so the teaching points in today's case are that heat stroke is a clinical diagnosis characterized by the presence of exposure to heat stress, CNS dysfunction, and a core temperature greater than 40.5 centigrade. It may be present in classic or exertional forms, but in either case, the patient may develop serious metabolic derangements and multi-organ failure. Treatment requires supportive care, prompt cooling, and dealing with the sequela of the multi-organ failure.

And you can find this question and other questions like it on Harrison Self-Review. And you can read more about this topic on the Harrison's chapter on heat-related illness. Visit the show notes for links to helpful resources, including related chapters and review questions from Harrison's, available exclusively on Access Medicine. If you enjoyed this episode, please leave us a review so we can reach more listeners just like you. Thanks so much for listening.