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Femoroacetabular impingement syndrome (FAI) is a pathologic entity which can lead to chronic symptoms of pain, reduced range of motion in flexion and internal rotation, and has been shown to correlate with degenerative arthritis of the hip. History, physical examination, and supportive radiographic findings such as evidence of articular cartilage damage, acetabular labral tearing, and early-onset degenerative changes can help physicians diagnose this entity. Several pathologic changes of the femur and acetabulum are known to predispose patients to develop FAI and recognition of these findings can ultimately lead to therapeutic interventions. The two basic mechanisms of impingement-cam impingement and pincer impingement-are based on the type of anatomic anomaly contributing to the impingement process. These changes can be found on conventional radiography, MR imaging, and CT examinations. However, the radiographic findings of this entity are not widely discussed and recognized by physicians. In this paper, we will introduce these risk factors, the proposed supportive imaging criteria, and the ultimate interventions that can help alleviate patients' symptoms.

Background: Chronic axial spinal pain is one of the major causes of significant disability and health care costs, with facet joints as one of the proven causes of pain. Objective: To provide evidence-based guidance in performing diagnostic and therapeutic facet joint interventions. Methods: The methodology utilized included the development of objectives and key questions with utilization of trustworthy standards. The literature pertaining to all aspects of facet joint interventions, was reviewed, with a best evidence synthesis of available literature and utilizing grading for recommendations. Summary of Evidence and Recommendations: Non-interventional diagnosis: • The level of evidence is II in selecting patients for facet joint nerve blocks at least 3 months after onset and failure of conservative management, with strong strength of recommendation for physical examination and clinical assessment. • The level of evidence is IV for accurate diagnosis of facet joint pain with physical examination based on symptoms and signs, with weak strength of recommendation. Imaging: • The level of evidence is I with strong strength of recommendation, for mandatory fluoroscopic or computed tomography (CT) guidance for all facet joint interventions. • The level of evidence is III with weak strength of recommendation for single photon emission computed tomography (SPECT) . • The level of evidence is V with weak strength of recommendation for scintography, magnetic resonance imaging (MRI), and computed tomography (CT) . Interventional Diagnosis: Lumbar Spine: • The level of evidence is I to II with moderate to strong strength of recommendation for lumbar diagnostic facet joint nerve blocks. • Ten relevant diagnostic accuracy studies with 4 of 10 studies utilizing controlled comparative local anesthetics with concordant pain relief criterion standard of ≥ 80% were included. • The prevalence rates ranged from 27% to 40% with false-positive rates of 27% to 47%, with ≥ 80% pain relief.Limitations: The limitations of these guidelines include a paucity of high-quality studies in the majority of aspects of diagnosis and therapy. Conclusions: These facet joint interventions guidelines were prepared with a comprehensive review of the literature with methodologic quality assessment with determination of level of evidence and strength of recommendations Key words: Chronic spinal pain, interventional techniques, diagnostic blocks, therapeutic interventions, facet joint nerve blocks, intraarticular injections, radiofrequency neurolysis

Milk-alkali syndrome can be caused by ingesting large amounts of calcium carbonate. Coincident with the promotion of calcium carbonate as treatment for both dyspepsia and osteoporosis, milk-alkali syndrome is now a common cause of hypercalcemia severe enough to require admission to the hospital. The syndrome accounted for less than 2% of such admissions before 1990, but from 1990 through 1993, it was the cause of hypercalcemia for over 12% of these patients. Only primary hyperparathyroidism and hypercalcemia of malignancy (excluding multiple myeloma) are more common. The diagnosis of milk-alkali syndrome is made almost entirely based on the patient's history; careful attention to dietary practices and over-the-counter drug use is required, as numerous over-the-counter medications contain calcium carbonate. Modern assays for PTH demonstrate the expected suppression of PTH by hypercalcemia. Nonetheless, measurement of PTH must be performed in a timely manner as treatment with intravenous saline may result in hypocalcemia and elevated PTH soon after admission. Given the pathophysiology of milk-alkali syndrome compared to other causes of hypercalcemia, hypocalcemia with rebound hyperparathyroidism is probably unique to milk-alkali syndrome.

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BACKGROUND CONTEXT: Current literature suggests that degenerated or damaged vertebral endplates are a significant cause of chronic low back pain (LBP) that is not adequately addressed by standard care. Prior 2-year data from the treatment arm of a sham-controlled randomized controlled trial (RCT) showed maintenance of clinical improvements at 2 years following radiofrequency (RF) ablation of the basivertebral nerve (BVN).

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Tears of the long head of the biceps tendon have a statistically significant association with tears of the anterior and superior rotator cuff and are highly correlated with tears of the supraspinatous and subscapularis tendons. When tears of these tendons are detected, specific attention directed toward the long biceps tendon is warranted to characterize the status of this structure that provides additional stability to the shoulder joint.