ABSTRACT
BACKGROUND: Necrotising fasciitis (NF) is a devastating disease with considerable mortality and morbidity, and early aggressive surgical debridement of devitalised necrotic tissues has traditionally been advocated. METHODS: We describe three patients who were referred from other units several weeks after developing periocular necrotising fasciitis; in all the three, the disease had been managed medically without surgical debridement, with apparent 'stalling' of the inflammatory process despite persistent necrotic periocular tissue. RESULTS: Following 'elective debridement' of the devitalised tissues and reconstruction with local flaps, all achieved a satisfactory aesthetic result. DISCUSSION: The role of host genetic determinants, polarised cytokine responses, and early, effective medical treatment in patients with atypical 'disease phenotypes' in NF are discussed.
Subject(s)
Eye Infections, Bacterial/therapy , Eyelid Diseases/therapy , Fasciitis, Necrotizing/therapy , Genetic Determinism , Orbital Diseases/therapy , Pseudomonas Infections/therapy , Streptococcal Infections/therapy , Aged , Anti-Bacterial Agents/therapeutic use , Blepharoplasty , Debridement , Eye Infections, Bacterial/drug therapy , Eye Infections, Bacterial/genetics , Eye Infections, Bacterial/surgery , Eyelid Diseases/drug therapy , Eyelid Diseases/genetics , Eyelid Diseases/surgery , Fasciitis, Necrotizing/drug therapy , Fasciitis, Necrotizing/genetics , Fasciitis, Necrotizing/surgery , Female , Humans , Male , Middle Aged , Orbital Diseases/drug therapy , Orbital Diseases/genetics , Orbital Diseases/surgery , Pseudomonas Infections/drug therapy , Pseudomonas Infections/genetics , Pseudomonas Infections/surgery , Streptococcal Infections/drug therapy , Streptococcal Infections/genetics , Streptococcal Infections/surgery , Surgical Flaps , Th1 Cells/immunology , Visual AcuityABSTRACT
Early effects of insulin and essential fatty acids on nerve conduction were studied. Insulin-dependent diabetes was induced in rats using streptozocin (65 mg/kg, i.p.); control rats were treated with buffer. Five weeks later, diabetic rats were divided into 5 groups. Two groups were given oral essential fatty acids (75% linoleic and 9% gamma-linolenic acids) for a further 3 and 5 days, respectively. Two other groups received subcutaneous insulin for a further 3 or 5 days. A group of diabetic rats were left without further treatment. Motor nerve conduction velocity was measured terminally in all rats by stimulating the sciatic nerve and recording EMGs in the gastrocnemius muscle under urethane anaesthesia. Sensory nerve conduction velocity was measured by stimulating and recording from the saphenous nerve trunk. Diabetic rats had significantly slowed motor and sensory nerve conduction velocities after 5 weeks (16.7%, P less than 0.001). Three days treatment with either insulin or fatty acids corrected the slowed motor nerve conduction velocity to a normal level. Conduction velocity in myelinated sensory nerves was still 10% slower in diabetic rats treated with insulin for 3 days (P less than 0.01). It was above the control level by 11% in diabetic rats treated with fatty acids for the same period (P less than 0.01). Conduction velocities in both sensory and motor nerves were normal in diabetic rats treated with either insulin or fatty acids for 5 days. It was concluded that both insulin and essential fatty acids had early effects on nerve conduction in diabetic rats. The speed of their actions, and the magnitudes of responses were different in sensory and motor nerves.
