The Place of Interventional Blocks in the Treatment of Avascular Necrosis Developing in Patients with Addison's Disease

Abstract

Introduction: Primary adrenal insufficiency (addison's disease) is associated with glucocorticoid deficiency.
Weight loss, orthostatic hypotension due to dehydration, hyponatremia, hyperkalemia, blood count disorders and hypoglycaemia are seen. The appropriate dose of glucocorticoid and minerocorticoid replacement should be applied in the treatment. Many risk factors, such as steroid therapy, are responsible for avascular necrosis in patients with Addison's disease. Here, we are presenting a case related to interventional blocks in the treatment of avascular necrosis which develops during Addison's disease treatment.
Case: 63 years old female patient. She has been monitored as an Addison's disease patient for 10 years and has a pain that is spreading downwards from the left hip for 5 years. She was using deltacortil 5 mg tb 1X1 for this Addison's disease. For the pain, she was admitted to various clinics for 5 years and lumbar disc herniation was diagnosed in the lumbar MR imaging, and operation for pregabalin 75 mg tb 2X1- initiated LDH was proposed, but as it was not accepted she was admitted to algology polyclinic. VAS was 9-10 when she came here. We told the patient to continue with previous treatments and suggested to apply an interventional block. First, caudal epidural block was applied, and she was told to come back 15 days later with hip MR imaging results. VAS was 6-7 in the control and avascular necrosis was found to be present in the left hip MR. After that, caudal epidural block + left femoral intraarticular injection was applied, and 15 days later caudal epidural block + left femoral intraarticular injection + left lumbar vertebral facet joint block was applied; and VAS was 1-2 in the control performed 15 days later. Then the previous 3 blocks were repeated, and treatment was ended with control to be performed 3 months later.
Conclusion: With the application of interventional block, sympathetic block, parasympathetic activity and vasodilatation develops here and oxygen increases in the damaged area. We think that the treatment here is associated with this mechanism.