Evaluation of the elderly patient with an abnormal gait

Distinguishing between the normal gait of the elderly and pathologic gaits is often difficult. Pathologic gaits with neurologic causes include frontal gait, spastic hemiparetic gait, parkinsonian gait, cerebellar ataxic gait, and sensory ataxic gait. Pathologic gaits with combined neurologic and musculoskeletal causes include myelopathic gait, stooped gait of lumbar spinal stenosis, and steppage gait. Pathologic gaits with musculoskeletal causes include antalgic gait, coxalgic gait, Trendelenburg gait, knee hyperextension gait, and other gaits caused by inadequate joint mobility. A working knowledge of the characteristics of these gaits and a systematic approach to observational gait examination can help identify the causes of abnormal gait. Patients with abnormal gait can benefit from the treatment of the primary cause of the disorder as well as by general fall-prevention interventions. Treatable causes of gait disturbance are found in a substantial proportion of patients and include normal-pressure hydrocephalus, vitamin B(12) deficiency, Parkinson's disease, alcoholism, medication toxicity, cervical spondylotic myelopathy, lumbar spinal stenosis, joint contractures, and painful disorders of the lower extremity.     

The Sigma-trial protocol: a prospective double-blind multi-centre comparison of laparoscopic versus open elective sigmoid resection in patients with symptomatic diverticulitis

Backround  

Diverticulosis is a common disease in the western society with an incidence of 33–66%. 10–25% of these patients will develop diverticulitis. In order to prevent a high-risk acute operation it is advised to perform elective sigmoid resection after two episodes of diverticulitis in the elderly patient or after one episode in the younger (< 50 years) patient. Open sigmoid resection is still the gold standard, but laparoscopic colon resections seem to have certain advantages over open procedures. On the other hand, a double blind investigation has never been performed. The Sigma-trial is designed to evaluate the presumed advantages of laparoscopic over open sigmoid resections in patients with symptomatic diverticulitis.     

The calcimimetic AMG 073 reduces parathyroid hormone and calcium x phosphorus in secondary hyperparathyroidism

BACKGROUND: A need exists for a therapy that lowers parathyroid hormone (PTH) without increasing calcium x phosphorus in patients with secondary hyperparathyroidism. The calcimimetic AMG 073 increases the sensitivity of the parathyroid calcium-sensing receptor to extracellular calcium, thereby reducing PTH secretion. Consequently, AMG 073 may provide a novel therapy for secondary hyperparathyroidism. METHODS: Seventy-eight hemodialysis patients with secondary hyperparathyroidism were enrolled into this 18-week, double-blind, randomized, placebo-controlled, dose titration study. Daily oral AMG 073 doses were administered to determine the effect on PTH, serum calcium, phosphorus, and calcium x phosphorus. RESULTS: The mean baseline PTH was similar in patients administered AMG 073 or placebo (632 +/- 280.1 pg/mL vs. 637 +/- 455.9 pg/mL, respectively). PTH decreased by 26.0% in the AMG 073-treated group, compared with an increase of 22.0% in the placebo group (P < 0.001). A greater proportion in the AMG 073 group (38%) had a decrease in PTH >or=30%, compared with the placebo group (8%) (P = 0.001). Decreases in PTH were independent of baseline vitamin D usage. Patients receiving AMG 073 had an 11.9% decrease in calcium x phosphorus compared with a 10.9% increase in the placebo group (P < 0.001). Use of vitamin D sterols, as well as both calcium and noncalcium-containing phosphate binders. were similar between treatment groups. Administration of AMG 073 was safe and well tolerated in this 18-week study. CONCLUSIONS: The calcimimetic AMG 073 decreases both PTH and calcium x phosphorus levels in hemodialysis patients with secondary hyperparathyroidism.     

外科手术中产生的烟气:仅仅是大量的热空气吗?

外科医生和手术室人员经常接触手术设备产生的烟气,病人也会暴露于烟气中,特别是腹腔镜手术中产生的烟气滞留于腹腔内这一密闭空间并被吸收.这些烟气是一种与香烟烟气相似的毒性物质,然而对这种毒性物质的影响还未引起足够重视.应该采取必要措施尽可能减少手术中烟气的不良影响.     

Biochemical and histological assessment of Alkali therapy during high animal protein intake in the rat

The Westernized diet is acidogenic due to the high content of sulfur-containing amino acids and relative deficiency of potassium organic anions. Chronic acid loads result in hypercalciuria and negative calcium balance often associated with loss of bone mineral. Alkali therapy tends to reverse the hypercalciuria but little is known regarding its effect on bone as assessed by bone histomorphometry. The present study utilized dynamic bone histomorphometry to evaluate the effects of alkali therapy on acid-induced changes in bone turnover. Serum and urine analyses and bone histomorphometry were assessed in adult rats after 2 months of either a low casein (LC) or high casein (HC) diet supplemented with either potassium chloride (KCl) or potassium citrate (KCit). Compared to animals on LC-KCl diet, HC-KCl diet delivered a substantial acid load as shown by significant increases in urinary sulfate, ammonium, and net acid excretion, and a lower urinary pH and citrate excretion without detectable changes in serum parameters. The acid load also resulted in hypercalciuria. Dynamic and static bone histomorphometry disclosed a significant reduction in cancellous bone volume and trabecular number associated with a 2.5-fold increase in eroded and a 3.5-fold increase in osteoclastic surfaces. There was also a near 2-fold increase in bone formation rate in rats on the HC-KCl diet. When animals on the HC diet were given KCit instead of KCl, all of the aforementioned changes in urine biochemistry and bone turnover were significantly attenuated or entirely prevented. These findings underscore the deleterious effects of high animal protein intake in promoting hypercalciuria and increasing bone turnover. Co-administration of potassium alkali attenuates or prevents these changes. In this animal model of high dietary animal protein intake, the major skeletal effect of alkali therapy is to reduce bone resorption, with little or no effect on bone formation.     

The role of vitamin D in vascular calcification in chronic kidney disease

Vascular calcification is a significant cause of morbidity and mortality in patients with chronic kidney disease (CKD). Disorders of mineral metabolism are likely involved in the pathogenesis of vascular calcification. Calcitriol and its analogs are effective in suppressing parathyroid hormone levels in patients with secondary hyperparathyroidism and CKD, but experimental studies demonstrate that these drugs can act directly on vascular smooth muscle cells. In some in vitro studies and in animal models of CKD, calcitriol has induced vascular calcification. Newer analogs of vitamin D appear to be less likely to induce vascular calcification, although published data are scarce. However, there is really no clear evidence in dialysis patients that calcitriol or analog administration is directly responsible for the induction of vascular calcification. However, indirectly, by oversuppression of parathyroid hormone (PTH) and induction of a low-turnover bone disease state, or by increased calcium-phosphorus product, the administration of calcitriol or its analogs may contribute to vascular calcification in patients with CKD. However, prospective randomized trials in CKD patients are necessary to fully understand the impact of calcitriol and analog therapy on vascular calcification.