Bruise colors vary from red, blue, or almost black, depending on the severity of broken capillaries or blood vessels within the bruise site. Broken venules or arterioles often result in a deep blue or dark red bruise, respectively. Darker colored bruises may result from a more severe bleeding from both blood vessels. Older bruises may appear yellow, green or brown. Cause
There are many causes of subcutaneous hematomas including ecchymoses. Coagulopathies such as Hemophilia A may cause ecchymosis formation in children. The medication betamethasone can have the adverse effect of causing ecchymosis.The presence of bruises may be seen in patients with platelet or coagulation disorders, or those who are being treated with an anticoagulant. Unexplained bruising may be a warning sign of child abuse, domestic abuse, or serious medical problems such as leukemia or meningoccocal infection. Unexplained bruising can also indicate internal bleeding or certain types of cancer. Long-term glucocorticoid therapy can cause easy bruising. Bruising present around the navel (belly button) with severe abdominal pain suggests acute pancreatitis. Connective tissue disorders such as Ehlers-Danlos syndrome may cause relatively easy or spontaneous bruising depending on the severity. Spontaneous bruising or bruising with minimal trauma in the absence of other explanations and together with other minor or major criteria suggestive of Vascular Ehlers-Danlos Syndrome (vEDS) suggests genetic testing for the condition.During an autopsy, bruises accompanying abrasions indicate the abrasions occurred while the individual was alive, as opposed to damage incurred post mortem.
Resistance
Resistance to aciclovir is rare in people with healthy immune systems, but is more common (up to 10%) in people with immunodeficiencies on chronic antiviral prophylaxis (transplant recipients, people with acquired immunodeficiency syndrome due to HIV infection). Mechanisms of resistance in HSV include deficient viral thymidine kinase; and mutations to viral thymidine kinase or DNA polymerase, altering substrate sensitivity. Microbiology
Aciclovir is active against most species in the herpesvirus family. In descending order of activity:
Herpes simplex virus type I (HSV-1)
Herpes simplex virus type II (HSV-2)
Varicella zoster virus (VZV)
Epstein–Barr virus (EBV)
Human cytomegalovirus (HCMV)  – least activity

Pharmacokinetics
Aciclovir is poorly water-soluble and has poor oral bioavailability (15–30%), hence intravenous administration is necessary if high concentrations are required. When orally administered, peak plasma concentration occurs after 1–2 hours. According to the Biopharmaceutical Classification System  (BCS),  aciclovir falls  under the BCS Class III drug i.e. soluble with low intestinal permeability. Aciclovir has a high distribution rate; protein binding is reported to range from 9 to 33%. The elimination half-life (t1/2) of aciclovir depends according to age group; neonates have a t1/2 of 4 hours, children 1–12 years have a t1/2 of 2–3 hours whereas adults have a t1/2 of 3 hours. Chemistry
Details of the synthesis of aciclovir were first published by scientists from the University at Buffalo. In the first step shown, 2,6-dichloropurine was alkylated with 1-benzoyloxy-2-chloromethoxyethane.