Differential hypertrophy and atrophy among all types of cutaneous innervation in the glabrous skin of the monkey hand during aging and naturally occurring type 2 diabetes.

Diabetic neuropathy (DN) is a common severe complication of type 2 diabetes. The symptoms of chronic pain, tingling, and numbness are generally attributed to small fiber dysfunction. However, little is known about the pathology among innervation to distal extremities, where symptoms start earliest and are most severe, and where the innervation density is the highest and includes a wide variety of large fiber sensory endings. Our study assessed the immunochemistry, morphology, and density of the nonvascular innervation in glabrous skin from the hands of aged nondiabetic rhesus monkeys and from age-matched monkeys that had different durations of spontaneously occurring type 2 diabetes. Age-related reductions occurred among all types of innervation, with epidermal C-fiber endings preferentially diminishing earlier than presumptive Adelta-fiber endings. In diabetic monkeys epidermal innervation density diminished faster, became more unevenly distributed, and lost immunodetectable expression of calcitonin gene-related peptide and capsaicin receptors, TrpV1. Pacinian corpuscles also deteriorated. However, during the first few years of hyperglycemia, a surprising hypertrophy occurred among terminal arbors of remaining epidermal endings. Hypertrophy also occurred among Meissner corpuscles and Merkel endings supplied by Abeta fibers. After longer-term hyperglycemia, Meissner corpuscle hypertrophy declined but the number of corpuscles remained higher than in age-matched nondiabetics. However, the diabetic Meissner corpuscles had an abnormal structure and immunochemistry. In contrast, the expanded Merkel innervation was reduced to age-matched nondiabetic levels. These results indicate that transient phases of substantial innervation remodeling occur during the progression of diabetes, with differential increases and decreases occurring among the varieties of innervation.

Risk stratification, perioperative and periprocedural management of the patient receiving anticoagulant therapy.

As a result of the aging US population and the subsequent increase in the prevalence of coronary disease and atrial fibrillation, therapeutic use of anticoagulants has increased. Perioperative and periprocedural management of anticoagulated patients has become routine for anesthesiologists, who frequently mediate communication between the prescribing physician and the surgeon and assess the risks of both thromboembolic complications and hemorrhage. Data from randomized clinical trials on perioperative management of antithrombotic therapy are lacking. Therefore, clinical judgment is typically needed regarding decisions to continue, discontinue, bridge, or resume anticoagulation and regarding the time points when these events should occur in the perioperative period. In this review, we will discuss the most commonly used anticoagulants used in outpatient settings and discuss their management in the perioperative period. Special considerations for regional anesthesia and interventional pain procedures will also be reviewed.

Preventing post-thoracotomy pain syndrome.

This article provides a concise overview of post-thoracotomy pain syndrome, describes anesthetic and surgical factors that have been investigated to reduce the incidence of the syndrome, and explores the effectiveness of various treatments for this condition. Although some interventions (both procedural and pharmacologic) have been investigated in both preventing and treating post-thoracotomy pain syndrome, definitive studies are lacking and firm conclusions regarding the benefit of any intervention cannot be drawn. The problem is compounded further by our lack of understanding of the pathophysiologic mechanisms underlying the development of chronic pain after surgery. Going forward, it will be important to elucidate these mechanisms and conduct well-designed trials involving novel therapeutic agents for both prevention and treatment of post-thoracotomy pain syndrome.