Increased skin temperature is commonly associated with erythermalgia. Erythromelalgia is a disorder caused by excessive vasodilation of the extremities and is characterized by paroxysmal redness, increased skin temperature and burning pain in a warm environment. Primary cases are more common. It is a rare disease. Patients are mostly children or 40 years old. The etiology and pathogenesis of the disease are still unclear. It is thought to be due to some disorder of the vasomotor center, so the involved sites are often symmetrically distributed. It is thought to be due to increased blood flow in the superficial and deep arteries of both limbs, resulting in increased skin circulation, redness and increased skin temperature. The dilated small blood vessels compress and stimulate the nerve endings, causing burning-like pain. It is also believed that the disease is associated with increased pentraxin in the peripheral circulation or the lack of countermechanism of normal vasoconstriction in the excessive response of the skin microvasculature to heat. In addition, the action of some harmful factors, such as chronic inflammation of the skin, UV damage, frost, burns and abrasions, can cause the loss of tension in the skin microvasculature and induce the disease. Occasionally, it is hereditary. The disease often has no obvious pathological anatomical changes and is not accompanied by local tissue organic abnormalities or nutritional changes. The disease mainly involves both feet at the same time, and a few only involve the soles of the feet, heels and toes, only 3.3% of the hands and feet at the same time, often symmetrical. The seizures depend on the skin temperature, which rises above a critical temperature (31.7-36.1°C), and the critical temperature point is fairly constant in all patients. Vasodilation and subsequent congestion are responsible for the increase in skin temperature. However, increased blood flow is not a major factor, as symptoms can persist once they are induced by warmth, i.e., when blood flow is reduced to 0 by pressurization above the systolic level using a pressure pulse band, suggesting that the lesion is due to abnormal sensitivity of skin nociceptive fibers to heat or tension in the dilated vessel wall. During the attack, the local capillaries are rapidly dilated and congested, the local skin temperature is increased (up to 35-37°C), and the dorsalis pedis and posterior tibial artery pulsations are enhanced.