Werner Ten Hoope1, Marjolein Looije, Philipp Lirk. 1. aDepartment of Anesthesiology, Academic Medical Center, University of Amsterdam, The Netherlands bDepartment of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Abstract
PURPOSE OF REVIEW: The aim of this review is to summarize recent relevant literature regarding regional anesthesia in the diabetic neuropathic patient and formulate recommendations for clinical practice. RECENT FINDINGS: Diabetic neuropathic nerves, but not nerves of diabetic patients per se, exhibit complex functional changes. As a result, they seem more sensitive to local anesthetics, and are more difficult to stimulate. When catheters are used postoperatively, diabetes is an independent risk factor for infection. SUMMARY: The pathophysiologic mechanisms underlying diabetic polyneuropathy are complex. Several pathways are thought to contribute to the development of diabetic neuropathy, triggered most importantly by chronic hyperglycemia. The latter induces inflammation and oxidative stress, causing microvascular changes, local ischemia and decreased axonal conduction velocity. Regional anesthesia is different in patients with diabetic neuropathy in several regards. First, the electric stimulation threshold of the nerve is markedly increased whereby the risk for needle trauma in stimulator-guided nerve blocks is theoretically elevated. Second, the diabetic nerve is more sensitive to local anesthetics, which results in longer block duration. Third, local anesthetics have been conjectured to be more toxic in diabetic neuropathy but the evidence is equivocal and should not be a cause to deny regional anesthesia to patients with a valid indication. Lastly, when peripheral nerve catheters are used, diabetes is an independent predisposing factor for infection.
PURPOSE OF REVIEW: The aim of this review is to summarize recent relevant literature regarding regional anesthesia in the diabetic neuropathicpatient and formulate recommendations for clinical practice. RECENT FINDINGS:Diabetic neuropathic nerves, but not nerves of diabeticpatients per se, exhibit complex functional changes. As a result, they seem more sensitive to local anesthetics, and are more difficult to stimulate. When catheters are used postoperatively, diabetes is an independent risk factor for infection. SUMMARY: The pathophysiologic mechanisms underlying diabetic polyneuropathy are complex. Several pathways are thought to contribute to the development of diabetic neuropathy, triggered most importantly by chronic hyperglycemia. The latter induces inflammation and oxidative stress, causing microvascular changes, local ischemia and decreased axonal conduction velocity. Regional anesthesia is different in patients with diabetic neuropathy in several regards. First, the electric stimulation threshold of the nerve is markedly increased whereby the risk for needle trauma in stimulator-guided nerve blocks is theoretically elevated. Second, the diabetic nerve is more sensitive to local anesthetics, which results in longer block duration. Third, local anesthetics have been conjectured to be more toxic in diabetic neuropathy but the evidence is equivocal and should not be a cause to deny regional anesthesia to patients with a valid indication. Lastly, when peripheral nerve catheters are used, diabetes is an independent predisposing factor for infection.