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J Dort

Publications and source records attributed to J Dort.

6 recordsLinked to original sources
PubMed1998

A prospective quantitative study of sensory deficits after whole sural nerve biopsies in diabetic and nondiabetic patients. Surgical approach and the role of collateral sprouting.

BACKGROUND: Sural nerve biopsy (Sbx) has been employed for the diagnosis of peripheral neuropathies and for multicenter trials of therapy in diabetic neuropathy. There is only limited prospective information available about what factors influence the resolution of the sensory deficit (Sdef) after biopsy. METHODS: We prospectively studied the surface area of skin Sdef after whole human Sbx in diabetic and nondiabetic patients for up to 18 months after the procedure. Sdef was determined by mapping, in two dimensions, the area of loss to pinprick and light touch in the sural distribution using a transparent boot-like device with 1-square-cm grid markings. At the same time, patients were interviewed about biopsy-related symptoms. RESULTS: Overall, the Sdef in all patients declined by an average of 91 +/- 3% at 18 months. The pattern of Sdef decline indicated that collateral sprouting was the mechanism of sensory reinnervation. The extent of Sdef at 6, 12, or 18 months did not differ between diabetics and nondiabetics. In diabetics, there was a correlation between sensory reinnervation with pre-biopsy sural nerve potential amplitude and HbA1C level, but not with age or diabetes duration. Diabetic patients who had nerve resections starting at or below the center of a plane through the lateral malleolus and traveling proximally for 7 cm or less had a Sdef that was less than patients with longer and more proximal nerve resections. The majority of patients had unpleasant but mild mechanically elicited sensory symptoms at 1 year that had improved in most, but not all patients, by 18 months. CONCLUSIONS: Sbx is associated with prolonged sensory symptoms and sensory loss. Recovery occurs by collateral reinnervation.

Biopsy↗
PubMed1997

Local human sural nerve blood flow in diabetic and other polyneuropathies.

Microangiopathy is considered relevant to the pathogenesis of several forms of peripheral nerve disease, particularly diabetic polyneuropathy. In diabetes, however, it is uncertain whether reductions in mixed nerve trunk blood flow account for early features of polyneuropathy in contrast to later disease, where microvascular changes have been described. To address this issue, we measured local sural nerve blood flow in patients with mild diabetic polyneuropathy who were enrolled in a clinical trial (n = 26), patients with other polyneuropathies being studied by diagnostic sural nerve biopsy (n = 17), patients with vasculitic polyneuropathy (n = 3) and one patient with rapidly progressive severe diabetic polyneuropathy and lumbosacral plexopathies. Standardized measurements were made at 10 sites along the sural nerve of each patient prior to sural nerve resection for biopsy. We used a laser Doppler flowmetry probe sensitive to red blood cell flux to measure sural nerve blood flow. This was slightly higher in patients with mild diabetes compared with those with other polyneuropathies, but was reduced in patients with vasculitis. In patients with mild diabetes, there was no relationship between sural nerve blood flow and prebiopsy sural nerve action-potential amplitude, sural myelinated fibre density, haemoglobin A1C, duration of diabetes or age of the patient. Ten diabetic patients entered in the clinical trial had sural nerve blood flow recorded in one sural nerve, followed 1 year later by a second sural nerve blood flow measurement prior to biopsy of the contralateral sural nerve. Despite a mild trend toward decline in fibre density between the nerves over this period of time, sural nerve blood flow was similar. The patient with severe diabetic polyneuropathy and lumbosacral plexopathies had reduced sural nerve blood flow. Our findings do not provide evidence that reductions in sural nerve blood flow are associated with early peripheral neuropathy in diabetes, unlike vasculitis. The early trend toward slight rises in sural nerve blood flow may be a result of early functional microangiopathy that accompanies nerve dysfunction but does not cause it.

Aged↗
PubMed1994

Liver transplantation for uncontrollable variceal bleeding.

OBJECTIVES: A small number of liver transplant candidates experience variceal bleeding that cannot be controlled by standard medical therapy. The objective of this study was to analyze the role of urgent liver transplantation for this subset of patients with acute, refractory, portal hypertensive bleeding. METHODS: Retrospective review of data from 416 patients undergoing 449 liver transplantations between March, 1988 and February, 1993 revealed seven patients (1.7%) with endstage liver disease who underwent transplantation for uncontrollable variceal bleeding. All patients failed therapy with intravenous pitressin, endoscopic sclerotherapy, balloon tamponade, and/or transjugular intrahepatic portosystemic shunt and continued to bleed. Patients ranged in age from 6 months to 56 years. All patients were Child's class C. Two patients were listed for transplantation with the United Network for Organ Sharing as status 3, and five patients were listed as status 4. RESULTS: All patients underwent successful liver transplantation with immediate control of bleeding. One patient expired on the 26th postoperative day from multiple organ failure, and another patient expired with recurrent hepatocellular carcinoma on the 110th postoperative day. No patients experienced late rebleeding from varices after transplantation. CONCLUSIONS: Urgent liver transplantation is effective and feasible for the small subset of patients with uncontrollable variceal bleeding and endstage liver disease. Prompt and complete evaluation of the potential recipient and availability of a donor organ are critical to the success of this approach.

Acute Disease↗