Norepinephrine increases thermogenesis in brown adipose tissue, and muscle contraction through shivering raises the metabolic rate.If these measures are insufficient to make the blood temperature in the brain match the new set point in the hypothalamus, the brain orchestrates heat effector mechanisms via the autonomic nervous system or primary motor center for shivering. These may be:
Increased heat production by increased muscle tone, shivering (muscle movements to produce heat) and release of hormones like epinephrine; and
Prevention of heat loss, e.g., through vasoconstriction.When the hypothalamic set point moves back to baseline—either spontaneously or via medication—normal functions such as sweating, and the reverse of the foregoing processes (e.g., vasodilation, end of shivering, and nonshivering heat production) are used to cool the body to the new, lower setting.This contrasts with hyperthermia, in which the normal setting remains, and the body overheats through undesirable retention of excess heat or over-production of heat. Hyperthermia is usually the result of an excessively hot environment (heat stroke) or an adverse reaction to drugs. Fever can be differentiated from hyperthermia by the circumstances surrounding it and its response to anti-pyretic medications.In infants, the autonomic nervous system may also activate brown adipose tissue to produce heat (non-exercise-associated thermogenesis, also known as non-shivering thermogenesis).Increased heart rate and vasoconstriction contribute to increased blood pressure in fever. Pyrogens
A pyrogen is a substance that induces fever. In the presence of an infectious agent, such as bacteria, viruses, viroids, etc., the immune response of the body is to inhibit their growth and eliminate them.
Superficial thrombophlebitis is a thrombosis and inflammation of superficial veins which presents as a painful induration with erythema, often in a linear or branching configuration forming cords. : 826–7 Superficial thrombophlebitis is due to inflammation and/or thrombosis, and less commonly infection of the vein. It is generally a benign, self-limited disorder, however, it can be complicated by deep vein thrombosis (DVT) and even pulmonary embolism (PE) Migratory superficial thrombophlebitis is known as Trousseaus syndrome. Signs and symptoms
Findings of tenderness, induration, pain and/or erythema along the course of a superficial vein usually establish a clinical diagnosis, especially in patients with known risk factors. In addition, there is often a palpable, sometimes nodular cord, due to thrombus within the affected vein. Persistence of this cord when the extremity is raised suggests the presence of thrombus. Complications
Superficial vein thrombosis extension to the deep vein system and/or recurrence of SVT. Suppurative thrombophlebitis is suspected when erythema extends significantly beyond the margin of the vein and is likely to be associated with significant fever. If suspected, antibiotic treatment, surgical drainage and potentially vein excision are indicated.Venous thromboembolism can occur with superficial vein thrombosis. Estimates of the percentage of patients with SVT who also have DVT vary between 6% and 53%, and symptomatic pulmonary embolism has been reported in 0% to 10% of patients with SVT. Risk factors
Patient characteristics and predisposing factors for thrombophlebitis nearly mirror those for DVT; thrombophlebitis is a risk factor for the development of DVT, and vice versa.