This results from the fact that these proteins have different half-lives: 1.5 to six hours for factor VII and eight hours for protein C, versus one day for factor IX, two days for factor X and two to five days for factor II. The larger the initial dose of vitamin K-antagonist, the more pronounced these differences are. This coagulation factor imbalance leads to paradoxical activation of coagulation, resulting in a hypercoagulable state and thrombosis. The blood clots interrupt the blood supply to the skin, causing necrosis. Protein C is an innate anticoagulant, and as warfarin further decreases protein C levels, it can lead to massive thrombosis with necrosis and gangrene of limbs. Notably, the prothrombin time (or international normalized ratio, INR) used to test the effect of warfarin is highly dependent on factor VII, which explains why patients can have a therapeutic INR (indicating good anticoagulant effect) but still be in a hypercoagulable state.In one third of cases, warfarin necrosis occurs in patients with an underlying, innate and previously unknown deficiency of protein C. The condition is related to purpura fulminans, a complication in infants with sepsis which also involves skin necrosis. These infants often have protein C deficiency as well. There have also been cases in patients with other deficiency, including protein S deficiency, activated protein C resistance (Factor V Leiden) and antithrombin III deficiency.Although the above hypothesis is the most commonly accepted, others believe that it is a hypersensitivity reaction or a direct toxic effect.
A compression fracture is a collapse of a vertebra. It may be due to trauma or due to a weakening of the vertebra (compare with burst fracture). This weakening is seen in patients with osteoporosis or osteogenesis imperfecta, lytic lesions from metastatic or primary tumors, or infection. In healthy patients, it is most often seen in individuals suffering extreme vertical shocks, such as ejecting from an ejection seat. Seen in lateral views in plain x-ray films, compression fractures of the spine characteristically appear as wedge deformities, with greater loss of height anteriorly than posteriorly and intact pedicles in the anteroposterior view. Signs and symptoms
Acute fractures will cause severe back pain. Compression fractures which develop gradually, such as in osteoporosis, may initially not cause any symptoms, but will later often lead to back pain and loss of height. Diagnosis
Compression fractures are usually diagnosed on spinal radiographs, where a wedge-shaped vertebra may be visible or there may be loss of height of the vertebra. In addition, bone density measurement may be performed to evaluate for osteoporosis. When a tumor is suspected as the underlying cause, or the fracture was caused by severe trauma, CT or MRI scans may be performed. Treatment
Conservative treatment
Back brace for support while the bone heals—either a Jewett brace for relatively stable and mild injuries, or a thoracic lumbar sacral orthosis (TLSO) for more severe ones. Opioids or non-steroidal anti-inflammatory drugs (NSAIDs) for pain. For osteoporotic patients, calcitonin may be helpful.