Heat Stroke: Impact On Blood Coagulation And Health

Heat stroke is a severe heat-related illness characterised by an elevation in body temperature, typically above 40°C, accompanied by clinical signs of central nervous system dysfunction. It is important to distinguish heat stroke from other heat-related illnesses, such as heat exhaustion and heat injury, as it can be life-threatening. A range of complications can arise from heat stroke, including coagulopathies, which refer to disorders of the blood's ability to clot and dissolve clots. This paragraph aims to explore the impact of heat stroke on coagulation and the underlying mechanisms involved.

Heat stroke can cause disseminated intravascular coagulation (DIC)

Heat stroke induces coagulofibrinolytic activation, which can lead to DIC. This activation causes both hypercoagulation and enhanced fibrinolysis. Fibrinolysis is the process of breaking down blood clots, and when this process is enhanced, it can lead to excessive bleeding. At the same time, hypercoagulation can cause blood to clot too much and too quickly, leading to blockages in blood vessels. This combination of enhanced fibrinolysis and hypercoagulation in DIC can be deadly.

The treatment strategy for DIC in heat stroke patients has not yet been established, and the time course of DIC in heat stroke has not been thoroughly evaluated. However, successful treatment of DIC in heat stroke patients has been reported. In one case, a combination of anticoagulant therapies was used to inhibit hypercoagulation and improve consumption coagulopathy, resulting in the resolution of DIC and a full recovery for the patient.

The presence of DIC in heat stroke patients is a significant prognostic factor for hospital mortality. A study of 705 heat stroke patients found that hospital mortality was significantly higher in those with DIC, with the risk of death increasing as the DIC score increased. Therefore, it is essential to monitor heat stroke patients for signs of DIC and provide appropriate treatment to improve outcomes.

Heat stroke can cause haemostasis breakdown

Endothelial damage caused by heat is believed to be the primary mechanism by which heat stroke induces platelet aggregation and microvascular thrombosis, resulting in consumptive coagulation. This, in turn, can lead to paradoxical bleeding when platelets are consumed faster than the body can produce them.

Heat stroke patients exhibit significant prolongation of prothrombin (PT), activated partial thromboplastin (aPTT), and thrombin times (TT), indicating disruptions in the coagulation process. In addition, they experience a significant reduction in plasma levels of antithrombin III (AT-III), factor V, proteins C and S, plasminogen activator inhibitor (PAI), and platelet count, further compromising their ability to maintain normal blood clotting.

The breakdown of haemostasis in heat stroke is multifactorial and can include thrombocytopenia, liver cell damage, and disseminated intravascular coagulation (DIC). DIC is a life-threatening condition where blood clots form throughout the microvasculature, resulting in a higher incidence of shock and increased mortality.

Heat stroke can cause endothelial damage, platelet aggregation and microvascular thrombosis

Heat stroke can cause endothelial damage, platelet aggregation, and microvascular thrombosis. These conditions can have severe consequences, including multiple organ failure and death.

Endothelial cells are susceptible to heat, and when affected, they release procoagulant factors such as von Willebrand factor (VWF) and factor VIII, suppress anticoagulant properties, and express adhesion molecules. This action promotes a prothrombotic state, which can lead to disseminated intravascular coagulation (DIC). DIC is a severe form of coagulopathy characterised by excessive clot formation and bleeding due to platelet depletion and dysfunction.

Heat can also directly affect platelet function, inducing cellular damage and loss of functional capacity. Platelets are involved in the pathogenesis of heat-related illness, and their activation plays a pivotal role in the development of coagulopathy. Heat stress can stimulate platelet aggregation by producing heat shock proteins (HSPs), which are essential for defending against thermal stress.

The delicate balance of coagulation enzymes, cellular receptors, and intracellular mechanisms is disrupted by hyperthermia, leading to a prothrombotic state and, in severe cases like heat stroke, consumption coagulopathy. This coagulopathy is characterised by the simultaneous appearance of intravascular thrombotic obstruction and increased bleeding tendency.

The breakdown of haemostasis in heat stroke is multifactorial and can include thrombocytopenia, liver cell damage, and DIC. Endothelial damage from heat is thought to cause downstream effects, resulting in platelet aggregation and microvascular thrombosis, which can lead to consumptive coagulation. This, in turn, can cause bleeding when platelets are used up faster than the body can produce them.

Heat stroke can cause bleeding

Heat stroke is a severe heat-related illness that involves a body temperature of over 40°C, as well as clinical signs of central nervous system dysfunction such as confusion, ataxia, delirium, or seizures. It is often brought on by strenuous physical activity or exposure to hot weather.

Heat stroke can cause a range of coagulopathies, from the activation of the coagulation cascade and fibrinolysis to fatal haemorrhaging or disseminated intravascular coagulation (DIC). Endothelial damage caused by heat is believed to cause platelet aggregation and microvascular thrombosis, which can lead to consumptive coagulation and, paradoxically, bleeding when platelets are used up faster than the body can produce them.

A study of 55 cases of heat stroke during the Makkah pilgrimage of 1983 found that 17 patients had disseminated intravascular coagulation (DIC). Those with DIC who also experienced bleeding had a higher incidence of shock and a higher mortality rate than non-bleeders. Thrombocytopenia and liver cell damage were also observed in some cases. The study concluded that the breakdown of haemostasis in heat stroke is multifactorial, involving thrombocytopenia, liver cell damage, and DIC.

Another study of 132 patients diagnosed with heat stroke during the pilgrimage to Makkah in 1989 and 1990 found significant alterations in coagulation and fibrinolysis. The study identified a reduction in plasma levels of antithrombin III (AT-III), factor V, proteins C and S, plasminogen activator inhibitor (PAI), and platelet count. These changes can increase the risk of bleeding and thrombus formation.

Overall, the available evidence suggests that heat stroke can cause bleeding through a combination of endothelial damage, platelet aggregation, microvascular thrombosis, and consumptive coagulation. The risk of bleeding is further compounded by alterations in coagulation factors and reduced platelet counts.

Heat stroke can cause thrombocytopenia and liver cell damage

Heat stroke is a severe heat-related illness that can be life-threatening and is characterised by an elevated body temperature of over 40°C and central nervous system dysfunction. Heat stroke can cause thrombocytopenia and liver cell damage, which can lead to disseminated intravascular coagulation (DIC).

Thrombocytopenia is a condition where there is a low number of platelets in the blood, and it is associated with systemic inflammatory response syndrome (SIRS) activation and poor prognosis in acute liver failure patients. Heat stroke can cause thrombocytopenia, which, in turn, is associated with a poor prognosis.

Heat stroke can also cause liver cell damage, which can be fatal. The liver is one of the first organs to be damaged by heat stroke, and it is often the site of fatal damage. The liver plays a vital role in metabolism, immunity, and excretion, and during heat stroke, it can undergo massive degeneration and hepatocellular necrosis.

The exact mechanisms of how heat stroke causes thrombocytopenia and liver cell damage are not yet fully understood, but several factors are believed to be involved. These include:

• Systemic factors such as heat cytotoxicity, coagulopathy, and SIRS.
• Excessive hepatocyte cell pyroptosis, which is a form of programmed cell death characterised by cell swelling and rapid plasma membrane rupture.
• Dysfunction of Kupffer cells, which are liver-resident macrophages that play a key role in maintaining liver homeostasis and clearing gut-derived endotoxins.
• Abnormal expression of heat shock proteins, which are highly conserved proteins that function as molecular chaperones and protect cells from heat injury.
• Activation of the coagulation cascade, leading to the formation of microthrombi and disseminated intravascular coagulation.
• Intestinal barrier dysfunction, which allows the translocation of endotoxins into the bloodstream, triggering SIRS and MODS.

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