: p.311  As a further complication, the nerves in the scrotal area are closely connected to those of the abdomen, sometimes causing abdominal pain similar to a hernia (see referred pain). Chronic epididymitis is most commonly associated with lower back pain, and the onset of pain often co-occurs with activity that stresses the low back (i.e., heavy lifting, long periods of car driving, poor posture while sitting, or any other activity that interferes with the normal curve of the lumbar lordosis region). : p.237

Treatment
In both the acute and chronic forms, antibiotics are used if an infection is suspected. The treatment of choice is often azithromycin and cefixime to cover both gonorrhoeae and chlamydia. Fluoroquinolones are no longer recommended due to widespread resistance of gonorrhoeae to this class. Doxycycline may be used as an alternative to azithromycin. In chronic epididymitis, a four- to six-week course of antibiotics may be prescribed to ensure the complete eradication of any possible bacterial cause, especially the various chlamydiae. For cases caused by enteric organisms (such as E. coli), ofloxacin or levofloxacin are recommended.In children, fluoroquinolones and doxycycline are best avoided. Since bacteria that cause urinary tract infections are often the cause of epididymitis in children, co-trimoxazole or suited penicillins (for example, cephalexin) can be used.Household remedies such as elevation of the scrotum and cold compresses applied regularly to the scrotum may relieve the pain in acute cases. Painkillers or anti-inflammatory drugs are often used for treatment of both chronic and acute forms.
Scott syndrome is a rare congenital bleeding disorder that is due to a defect in a platelet mechanism required for blood coagulation.Normally when a vascular injury occurs, platelets are activated and phosphatidylserine (PS) in the inner leaflet of the platelet membrane is transported to the outer leaflet of the platelet membrane, where it provides a binding site for plasma protein complexes that are  involved in the conversion of prothrombin to thrombin, such as factor VIIIa-IXa (tenase) and factor Va-Xa (prothrombinase).In Scott syndrome, the mechanism for translocating PS to the platelet membrane is defective, resulting in impaired thrombin formation. A similar defect in PS translocation has also been demonstrated in Scott syndrome red blood cells and Epstein–Barr virus transformed lymphocytes, suggesting that the defect in Scott syndrome reflects a mutation in a stem cell that affects multiple hematological lineages.The basis for the defect in PS translocation is, at present, unknown. A candidate protein, scramblase, that may be involved in this process appears to be normal in Scott syndrome platelets. Other possible defects in PS translocation, reported in some patients, require further study. The initially reported patient with Scott Syndrome has been found to have a mutation at a splice-acceptor site of the gene encoding anoctamin 6 (ANO6, transmembrane protein 16F, TMEM16F). At present, the only treatment for episodes of bleeding is the transfusion of normal platelets. References
Further reading
Heemskerk JWM, Bevers EM, Lindhout T. Platelet activation and blood coagulation, Thromb Haem 2002; 88:186–194
Martinez MC, Martin S, Toti F, Fressinaud E, Dachary-Prigent J, Meyer D, et al.