Bleeding farther back in the nose is known as a posterior bleed and is usually due to bleeding from Woodruffs plexus, a venous plexus situated in the posterior part of inferior meatus. Posterior bleeds are often prolonged and difficult to control. They can be associated with bleeding from both nostrils and with a greater flow of blood into the mouth. Sometimes blood flowing from other sources of bleeding passes through the nasal cavity and exits the nostrils. It is thus blood coming from the nose but is not a true nosebleed, that is, not truly originating from the nasal cavity. Such bleeding is called "pseudoepistaxis" (pseudo + epistaxis). Examples include blood coughed up through the airway and ending up in the nasal cavity, then dripping out. Prevention
People with uncomplicated nosebleeds can use conservative methods to prevent future nosebleeds such as sleeping in a humidified environment or applying petroleum jelly to the nasal nares. Treatment
Most anterior nosebleeds can be stopped by applying direct pressure, which helps by promoting blood clots. Those who have a nosebleed should first attempt to blow out any blood clots and then apply pressure for at least five minutes and up to 20 minutes. Pressure should be firm and tilting the head forward helps decrease the chance of nausea and airway obstruction as seen in the picture on the right. When attempting to stop a nosebleed at home, the head should not be tilted back. Swallowing excess blood can irritate the stomach and cause vomiting.
The activated Factor IXa with Factor VIIIa forms the "tenase" complex. This "tenase" complex activates more Factor X, which in turn forms new prothrombinase complexes with Factor Va. Factor Xa is the prime component of the prothrombinase complex which converts large amounts of prothrombin—the "thrombin burst". Each molecule of Factor Xa can generate 1000 molecules of thrombin. This large burst of thrombin is responsible for fibrin polymerization to form a thrombus. Factor Xa also plays a role in other biological processes that are not directly related to coagulation, like wound healing, tissue remodelling, inflammation, angiogenesis and atherosclerosis. Inhibition of the synthesis or activity of Factor X is the mechanism of action for many anticoagulants in use today. Warfarin, a synthetic derivative of coumarin, is the most widely used oral anticoagulant in the US. In some European countries, other coumarin derivatives (phenprocoumon and acenocoumarol) are used. These agents known as vitamin K antagonists (VKA), inhibit the vitamin K-dependent carboxylation of Factors II (prothrombin), VII, IX, X in the hepatocyte. This carboxylation after the translation is essential for the physiological activity.Heparin (unfractionated heparin) and its derivatives low molecular weight heparin (LMWH) bind to a plasma cofactor, antithrombin (AT) to inactivate several coagulation factors IIa, Xa, XIa and XIIa. The affinity of unfractionated heparin and the various LMWHs for Factor Xa varies considerably. The efficacy of heparin-based anticoagulants increases as selectivity for Factor Xa increases.