Pleural fluid can dilute hemothoraces in as low as 3–4 days. The red blood cells in the effusion spontaneously break down. Distinguishing the pleural fluid from blood by colour is impossible when the hematocrit value is over 5%. For these reasons, even if there is a hematocrit value under 50%, further investigations can be done in order to figure out if there is a source of bleeding. Hematocrit can be roughly calculated by dividing the red blood cell count of the pleural fluid by 100,000. Thoracentesis is the test most commonly used to diagnose a hemothorax in animals. Hemothorax can itself be a rare complication of thoracentesis if the intercostal artery is punctured. Treatment
The treatment of a hemothorax depends largely on the extent of bleeding. While small hemothoraces may require little in the way of treatment, larger hemothoraces may require fluid resuscitation to replace the blood that has been lost, drainage of the blood within the pleural space using a procedure known as a tube thoracostomy, and potentially surgery in the form of a thoracotomy or video-assisted thoracoscopic surgery (VATS) to prevent further bleeding. Occasionally, transcatheter arterial embolization may be used to stop ongoing arterial bleeding. Additional treatment options include antibiotics to reduce the risk of infection and fibrinolytic therapy to break down clotted blood within the pleural space. Thoracostomy
Blood in the cavity can be removed by inserting a drain (chest tube) in a procedure called a tube thoracostomy.
The mutations are mainly missense mutations with nonsense and Frameshift mutations each occurring in 12.5% of cases. The causes of two fibrinogen abnormalities that characterize hypodysfibrinogenemia, i.e. circulation at reduced levels of fibrinogen at least some of which is dysfunctional, reflect different molecular mechanisms:
A heterozygous mutation in one of the two copies of either the FGA, FGB, or FGG gene leads to production of a fibrinogen that is both dysfunctional and poorly secreted into the blood stream, e.g. fibrinogen Vlissingen, fibrinogen Philadelphia, and fibrinogen Freiburg. A homozygous mutation in both copies of one of the cited genes leads to production of a fibrinogen that is both dysfunctional and poorly secreted into the blood stream, e.g. fibrinogen Otago,  fibrinogen Marburg, and fibrinogen Sfax. Two different mutations (see Compound heterozygosity) occur in each of the two copies of one of the cited genes, with one mutation coding for reduced formation of a functionally normal circulating fibrinogen and the second mutation coding for the circulation of a dysfunctional fibrinogen, e.g. fibrinogen Leipzig. Two different mutations occur in one copy of the cited genes, with one mutation causing hypofibrinogenemia and the other mutation coding for a dysfunctional fibrinogen, e.g. fibrinogen Keokuk.The following Table adds further information on the just cited examples of hypodysfibrinogenemias. The Table gives: a) each mutated proteins trivial name; b) the gene mutated (i.e. FGA, FGB, or FGG), its mutation site (i.e. numbered nucleotide in the cloned gene), and name of the nucleotides (i.e.