Search

Surgical intervention is an integral component in the diagnosis and management of mycetoma. Surgical treatment is indicated for small, localised lesions and massive lesions to reduce the mycetoma load and to enable better response to medical therapy. It is also a life-saving procedure in patients with massive disease and sepsis. Surgical options for mycetoma treatment range from a wide local surgical excision to repetitive debridement excisions to amputation of the affected part. Adequate anaesthesia, a bloodless field, wide local excision with adequate safety margins in a suitable surgical facility, and expert surgeons are mandatory to achieve the best surgical outcome. Surgical intervention in mycetoma is associated with considerable morbidity, deformities, and disabilities, particularly in advanced disease. These complications can be reduced by educating patients to seek medical advice earlier when the lesion is small, localised, and amenable to surgery. There is no evidence for mycetoma hospital cross infection. This communication is based on the authors’ experience in managing over 7,200 mycetoma patients treated at the Mycetoma Research Centre, University of Khartoum, Sudan. [ABSTRACT FROM AUTHOR]

Objective: We aimed to investigate neurophysiological and clinical effects of common krait envenoming, including the time course and treatment response. Methodology: Patients with definite common krait (Bungarus caeruleus) bites were recruited from a Sri Lankan hospital. All patients had serial neurological examinations and stimulated concentric needle single-fibre electromyography (sfEMG) of orbicularis oculi in hospital at 6wk and 6–9mth post-bite. Principal Findings: There were 33 patients enrolled (median age 35y; 24 males). Eight did not develop neurotoxicity and had normal sfEMG. Eight had mild neurotoxicity with ptosis, normal sfEMG; six received antivenom and all recovered within 20–32h. Seventeen patients developed severe neurotoxicity with rapidly descending paralysis, from ptosis to complete ophthalmoplegia, facial, bulbar and neck weakness. All 17 received Indian polyvalent antivenom a median 3.5h post-bite (2.8–7.2h), which cleared unbound venom from blood. Despite this, the paralysis worsened requiring intubation and ventilation within 7h post-bite. sfEMG showed markedly increased jitter and neuromuscular blocks within 12h. sfEMG abnormalities gradually improved over 24h, corresponding with clinical recovery. Muscle recovery occurred in ascending order. Myotoxicity was not evident, clinically or biochemically, in any of the patients. Patients were extubated a median 96h post-bite (54–216h). On discharge, median 8 days (4–12days) post-bite, patients were clinically normal but had mild sfEMG abnormalities which persisted at 6wk post-bite. There were no clinical or neurophysiological abnormalities at 6–9mth. Conclusions: Common krait envenoming causes rapid onset severe neuromuscular paralysis which takes days to recover clinically consistent with sfEMG. Subclinical neuromuscular dysfunction lasts weeks but was not permanent. Antivenom effectively cleared venom but did not prevent worsening or reverse neuromuscular paralysis. [ABSTRACT FROM AUTHOR]