Do surgical site complications after ankle fracture surgery reduce with Aquacel Extra Ag®? / ¿Disminuyen las complicaciones cutáneas tras la cirugía de fracturas de tobillo con el uso de Aquacel Extra Ag®?

INTRODUCTION: Ankle fractures account for up to 10% of total fractures. Most of them require surgical fixation, which involves an important risk of wound complications. The aim of this study was to determine whether a silver-impregnated occlusive surgical dressing (Aquacel Ag Extra®) was effective in reducing the rates of wound complications after ankle fracture open reduction and internal fixation compared to standard sterile dressing. METHODS: We prospectively reviewed 233 patients who underwent ankle fracture open reduction and internal fixation. Surgeons switched from using a standard dressing to an Aquacel Ag Extra® from July 2017 to February 2018, without other major changes in perioperative management. We compared skin complications between both groups after 3 months' follow-up. RESULTS: The statistical analysis showed that there is no difference in the prevalence of skin complications between both groups. CONCLUSIONS: The theoretical advantages of silver impregnated dressings need further prospective randomized controlled studies to assess the appropriate indications for their use in orthopaedic surgery.

Molecular genetic advances in neurodegenerative disorders.

Advances in molecular genetics have had a major impact on our understanding of the pathogenesis of neurologic disorders. This article discusses molecular genetic contributions to our knowledge of Huntington's disease, amyotrophic lateral sclerosis, and Alzheimer's disease, as well as their implications for diagnosis and treatment. Specific, sensitive testing for Huntington's disease is now possible; elucidation of the pathogenesis of familial amyotrophic lateral sclerosis has been achieved and has launched promising drug trials; and the heterogeneity and pathogenetic complexity of Alzheimer's disease have been revealed.

Low diagnostic yield of sural nerve biopsy in patients with peripheral neuropathy and primary amyloidosis.

Patients with primary amyloidosis may develop peripheral neuropathy as an early feature. Sural nerve biopsy is reported to be a sensitive method for diagnosing amyloidosis in such patients. We identified nine patients, ultimately diagnosed as having amyloidosis, who were referred for peripheral neuropathy of undetermined etiology. In six, a sural nerve biopsy demonstrated no amyloid. Subsequent examination of other tissue or of the contralateral sural nerve eventually resulted in the correct diagnosis. We conclude that sural nerve biopsy may be less sensitive than previously believed for the diagnosis of amyloidosis in patients with peripheral neuropathy secondary to amyloid. When the clinical suspicion of amyloidosis is high, a nondiagnostic sural nerve biopsy should not discourage the performance of further investigative studies.

Quantitative histopathology of the inflammatory myopathies.

This study quantitatively assessed skeletal muscle histopathology in 57 patients with inflammatory myopathy, including 20 patients with polymyositis (PM), 19 patients with dermatomyositis (DM), and 18 patients with evidence of an additional connective-tissue disease. No histologic criteria for invariably distinguishing patients with inflammatory myopathy were established because of overlap in individual measurements, but general histopathologic distinctions were confirmed. In PM, endomysial mononuclear cell infiltration (fibers bordering on inflammation) was usual, whereas in DM inflammation of large vessels, fibers with circumscribed areas of myofibrillar loss, and perifascicular atrophy were seen. Patients with evidence of an additional connective-tissue disease were most similar to the DM patients, with a greater prevalence of perivascular inflammation than in the PM patients. Because of varying histopathology (and presumed varying pathogenesis), future therapeutic trials would be more informative if they were designed using patients with homogeneous histologic features.

Lymphocytaplasmapheresis in Devic's syndrome.

A pregnant 26-year-old woman with Devic's syndrome manifesting as paraplegia and visual loss was treated with multiple courses of lymphocytaplasmapheresis. Clinical improvement was temporally related to the lymphocytaplasmapheresis. She relapsed when treatment was stopped and improved with reinstitution of therapy. Thereafter, further treatments were not required and she delivered a normal infant.

Meningeal carcinomatosis from an ovarian primary: a clinicopathologic study.

Meningeal carcinomatosis due to primary ovarian carcinoma is an uncommon metastasis that presents difficult problems in diagnosis and management of patients known to have this disease. There is evidence that extended survival due to advances in treatment of ovarian carcinoma has improved our ability to diagnose meningeal carcinomatosis of this tumor more often. Herein the first case of meningeal metastasis of primary ovarian cancer with cytologic and postmortem examination is discussed.

Effect of magnesium on sodium transport in toad urinary bladder.

Voltage-clamp techniques were employed to examine the effect of magnesium (Mg) on sodium transport in the isolated urinary bladder of the Dominican toad. Substitution of 1 mM Mg had no effect, but 3-mM Mg substitution resulted in a reversible increase in short-circuit current (27%) and potential difference (19%) and decrease in transepithelial resistance (14%); no greater effect was seen with 5- or 10-mM Mg substitution. The effect was produced by mucosal or mucosal and serosal Mg substitution; serosal Mg substitution was without effect. Analysis of electrical parameters disclosed that magnesium increased net sodium transport via an effect on the sodium pump.

Neurogenic control of renal tubular sodium reabsorption in the dog: a brief review and preliminary report concerning possible humoral mediation.

The evidence supporting a role for direct neurogenic control of renal tubular sodium reabsorption is reviewed. Electron microscopic and fluorescence histochemical studies have demonstrated adrenergic nerve terminals in direct contact with basement membranes of mammalian renal tubular epithelial cells. Low level direct or baroreceptor reflex stimulation of renal sympathetic nerves produces an increase in renal tubular sodium reabsorption without alterations in glomerular filtration rate, renal blood flow, or intrarenal distribution of blood flow. The antinatriuresis was prevented by prior treatment of the kidney with guanethidine or phenoxybenzamine. Rat kidney micropuncture studies have localized the site of enhanced tubular sodium reabsorption to the proximal tubule. Possible indirect mediation of the antinatriuresis by other humoral agents known to be released from the kidney upon renal nerve stimulation was explored. Renal blockade to circulating angiotensin II did not alter the antinatriuretic response to low level direct renal nerve stimulation. Indomethacin was used to inhibit prostaglandin synthesis; this resulted in a rise in mean arterial pressure, a fall in renal blood flow, no significant change in glomerular filtration rate, and a variable fall in urinary sodium excretion. Despite inhibition of prostaglandin synthesis, low level direct renal nerve stimulation produced an increase in renal tubular sodium reabsorption in the absence of changes in renal hemodynamics. Thus, the antinatriuresis of low level direct renal nerve stimulation is not mediated by either circulating angiotensin II or prostaglandin.

Renal neuroadrenergic transmission.

To study the role of the renal sympathetic nerves in the regulation of sodium excretion, we examined the renal functional response to left renal nerve stimulation before (group I) and after (group II) left renal adrenergic blockade with guanethidine. In group I dogs, absolute sodium excretion from the left kidney fell markedly after left renal nerve stimulation; the decreases in glomerular filtration rate and renal blood flow were of a similar magnitude. Using the radiolabeled microsphere technique, distribution of renal blood flow to the outer cortex was diminished after left renal nerve stimulation. In group II dogs, guanethidine blocked all of these effects of left renal nerve stimulation. In group iii studies, a low level of left renal nerve stimulation was used which resulted in a decrease in sodium excretion in the absence of changes in glomerular filtration rate, renal blood flow, or intrarenal distribution of blood flow; this effect was blocked by renal adrenergic blockade with guanethidine in group iv studies. These data support a role for the renal sympathetic nerves to directly influence renal tubular sodium transport in the absence of alterations in renal hemodynamics.