Heat stroke is a life-threatening condition characterised by hyperthermia and multiple organ failure. Although mild to moderate hepatocellular injury is a common complication, severe liver injury and acute liver failure are rare. The prognosis of heat stroke depends on how early it is diagnosed and treated with appropriate measures, including cooling methods and the correction of water and electrolyte balance. This article will explore the relationship between heat stroke and liver damage, discussing cases of varying severity and outcomes.
Characteristics | Values |
---|---|
Heat stroke | A life-threatening condition characterised by hyperthermia and multiple organ failure |
Hepatocellular injury | A well-documented complication of heat stroke |
Mild to moderate hepatocellular injury | Common |
Severe liver injury | Rare |
Acute liver failure | Rare |
Treatment | Fast and effective cooling, conservative treatment, liver transplantation |
Cooling methods | Cold fluids, cold water immersion, application of ice packs, cold packs or wet gauze sheets |
Antipyretics | Ineffective and can even aggravate coagulopathy and liver injury |
What You'll Learn
Heat stroke and hyperpyrexia
Heat stroke is a life-threatening condition characterised by hyperthermia and multiple organ failure. Hyperpyrexia is a core body temperature of over 40°C. Heat stroke can be caused by exposure to high environmental temperatures (classic heat stroke) or from strenuous physical activity (exertional heat stroke).
Hepatocellular damage is an invariable complication of heat stroke, although it is usually mild or moderate and can only be detected through biochemical testing or a liver biopsy. In rare cases, severe liver damage can occur and contribute to a fatal outcome. In these cases, liver transplantation may be required, although conservative treatment has been successful in some patients.
The pathologic changes to the liver caused by heat stroke include centrolobular degeneration or necrosis of hepatocytes and congestion; cholestasis and portal venular dilatation are common in fatal cases. It is suggested that these changes are the result of a combination of hypoxia and direct thermal injury.
Stroke Recovery: Returning to Work?
You may want to see also
Heat stroke and hypoxia
Heat stroke is a form of hyperthermia associated with a systemic inflammatory response that leads to multiorgan dysfunction syndrome (MODS). The hypothalamus is believed to be involved in regulating homeostasis, motivation, and emotional behaviour by controlling autonomic and endocrine activity. The hypothalamus communicates input from the thalamus to the pituitary gland, reticular activating substance, limbic system, and neocortex. This allows the output of pituitary hormones to respond to changes in the autonomic nervous system activity and to the needs of temperature regulation, water balance, and energy requirements.
Heat exposure is a stimulus that triggers biological stress reactions. An increase in c-fos mRNA and protein in different brain regions, including the hypothalamus, the thalamus, and the amygdala, occurs in heat-exposed rats. Large releases of hippocampal norepinephrine, hypothalamic dopamine and serotonin, and striatal glutamate have also been reported. The hypothalamic paraventricular nucleus has been described as the "autonomic master controller". It coordinates critical physiological responses by controlling the hypothalamic-pituitary-adrenocortical (HPA) axis.
Heat stroke can be caused by severe heat exposure (classic heat stroke) or strenuous work (exertional heat stroke). It is characterised by a myriad of inflammation, coagulation, and tissue injuries. Heat stroke is a medical emergency that requires prompt intervention. The classic syndrome of heat stroke is a manifestation of critical hyperthermia with neurological decompensation that results in delirium, convulsion, or coma.
The hypothalamus may be involved in regulating homeostasis, motivation, and emotional behaviour. These functions are mediated through hypothalamic control of autonomic and endocrine activity. The hypothalamus receives input from the thalamus, reticular activating substance, limbic system, eyes, and neocortex; it then transmits this input to the pituitary gland. This allows the output of pituitary hormones to respond to changes in the autonomic nervous system activity and to the needs of temperature regulation, water balance, and energy requirements.
The major heat stroke syndromes include hyperthermia, hypotension, intracranial hypertension, and hypothalamic ischemia and hypoxia. After the onset of heat stroke, neuronal necrosis, apoptosis, and autophagy also occur in the hypothalamus.
Stroke Patients' Oxygen Needs: Understanding the Why
You may want to see also
Heat stroke and hepatic encephalopathy
Heat stroke is a life-threatening condition characterised by hyperthermia and multiple organ failure. Hepatic encephalopathy is brain dysfunction caused by liver dysfunction. It is caused by neurotoxins in the blood that are usually filtered by the liver. Heat stroke can cause mild to moderate hepatocellular injury, which can develop into acute liver failure. This, in turn, can lead to hepatic encephalopathy.
Hepatic encephalopathy can manifest in a wide variety of ways, affecting mood, personality, behaviour, memory, concentration, thinking, consciousness, sleep patterns, coordination, and motor functions. Symptoms may occur suddenly or gradually and can be mild or severe.
The West Haven Criteria is the most common grading system for categorising the severity of hepatic encephalopathy. It grades symptoms on a scale of 0 to 4, with stages 0 to 1 considered minimal hepatic encephalopathy and stages 2 to 4 considered overt hepatic encephalopathy.
The treatment for hepatic encephalopathy includes managing urgent conditions that may have triggered it, treating the underlying cause, and reducing neurotoxin levels in the blood. Antibiotics and osmotic laxatives are often used to reduce neurotoxin levels.
While hepatic encephalopathy can get better with treatment, it can be life-threatening if left untreated. Therefore, it is important to seek medical attention as soon as possible to prevent the condition from worsening or causing permanent damage.
Chocolate's Benefits for Stroke Patients: What You Need to Know
You may want to see also
Heat stroke and coagulopathy
Heat stroke is a life-threatening condition characterised by hyperthermia and multiple organ failure. Hepatic injury is a well-documented complication of heat stroke, but severe liver injury and acute liver failure are rare.
Heat stroke-induced coagulopathy (HSIC) is a coagulopathy with diagnostic features similar to disseminated intravascular coagulopathy (DIC). It occurs early after heat exposure and before tissue-level histopathological changes in end-organs can be observed. HSIC is a prime candidate for the mechanism of the increased risk of heat stroke-related pathology following bacterial or viral infection.
Coagulation markers may serve as accessible biomarkers for heat stroke severity and therapeutic strategies. A mouse model of classic heat stroke revealed that prior viral infection simulated with poly I:C injection resulted in heat stroke presenting with high levels of factors indicating coagulopathy. Despite a decreased number of platelets in the blood, the platelets were large and non-uniform in size, suggesting younger, more active platelets.
In a study of 302 patients with heat illness, 131 (43.4%) suffered from heat stroke, including 7 deaths (5.3%). Core temperature, prothrombin time, and D-dimer were independent risk factors for heat stroke, and were used to construct a heatstroke-induced coagulopathy (HIC) scoring system. A total score of ≥3 indicated HIC, and HIC scores correlated with the score for International Society of Thrombosis and Hemostasis-DIC. The incidence of HIC (27.5%) was higher than that of DIC (11.2%) in all 131 heat stroke patients.
The early use of fibrinogen replacement may serve as a therapeutic intervention to alleviate platelet hyporeactivity and prevent complications in patients with heat stroke.
How Can Someone Cause Another Person to Have a Stroke?
You may want to see also
Heat stroke and hypercoagulability
Heat stroke is a life-threatening condition characterised by hyperthermia and multiple organ failure. It can be caused by exposure to high environmental temperatures or strenuous physical activity, particularly in hot environments.
Heat stroke is associated with hypercoagulability, which is the tendency for the blood to form clots too easily. Hypercoagulability can lead to disseminated intravascular coagulation (DIC) and multiple organ failure. Inflammation and coagulation are the two major factors that provoke life-threatening organ dysfunction in heat stroke.
Heat stroke-induced hypercoagulability can be caused by a combination of hypoxia and direct thermal injury. It can also be caused by systemic inflammation, which is triggered by damage-associated molecular patterns (DAMPs) that bind to receptors and upregulate inflammation through inflammasome formation. This inflammatory response may be mediated by the molecular chaperone family of heat shock proteins.
Heat stroke-induced hypercoagulability can also be caused by rhabdomyolysis, which is the breakdown of skeletal muscle due to damage to muscle cells. Rhabdomyolysis can release myoglobin, which is toxic to the kidneys and can cause acute kidney injury.
The treatment for heat stroke includes rapid cooling and rehydration. In some cases, anticoagulant therapy may be used to manage hypercoagulability, although the evidence for this is limited.
Stroke Victims: Consciousness and the Recovery Process
You may want to see also
Frequently asked questions
Heat stroke is a life-threatening condition characterised by hyperthermia and multiple organ failure.
Yes, heat stroke can cause mild to moderate hepatocellular injury. However, severe liver injury and acute liver failure are rare.
Conservative treatment is the cornerstone of treatment for liver damage caused by heat stroke. Fast and effective cooling is essential, along with support for organ dysfunction. In some cases, liver transplantation may be required.