Abstract

Necrotizing myositis is a rare and fatal disease of skeletal muscles caused by group A beta hemolytic streptococci (GABHS). Its early detection by advanced imaging forms the basis of current management strategy. Paucity of advanced imaging in field/rural hospitals necessitates adoption of management strategy excluding imaging as its basis. Such a protocol, based on our experience and literature, constitutes:i. Prompt recognition of the clinical triad: disproportionate pain; precipitous course; and early loss of power- in a swollen limb with/without preceding trauma.ii. Support of clinical suspicion by 2 ubiquitous laboratory tests: gram staining- of exudates from bullae/muscles to indicate GABHS infection; and CPK estimation- to indicate myonecrosis.iii. Replacement of empirical antibiotics with high intravenous doses of sodium penicillin and clindamyciniv. Exploratory fasciotomy: to confirm myonecrosis without suppuration- its hallmarkv. Emergent radical debridementvi. Primary closure with viable flaps – unconventional, if need be.

Highlights

  • Necrotizing myositis (NM) is a rare disease of skeletal muscles caused by group A beta hemolytic streptococcus (GABHS) [1]

  • Urgent bed side fasciotomy (Figs. 1 &2) revealed extensive myonecrosis sparing the anterior compartment of thigh

  • GABHS cultured from the excised muscles were sensitive to penicillin, clindamycin and amikacin

Read more

Summary

Introduction

Necrotizing myositis (NM) is a rare disease of skeletal muscles caused by group A beta hemolytic streptococcus (GABHS) [1]. Exploratory fasciotomy revealed myonecrosis of the entire lower limb sparing the gluteal compartment, with conspicuously absent pus. Isolation of streptococci (signifying GABHS infection) coupled with raised CPK (signifying myonecrosis) is, in our opinion, indicator enough for adoption of aggressive surgical management and change to high doses of specific antibiotics- combination of sodium penicillin and clindamycin [4], from empirically commenced ones. Additional incisions on the muscles confirm the absence of perfusion due to obliteration of muscular arteries by leucocytic infiltration This simple procedure clinches the diagnosis, and relieves the compartment pressures, decelerating the rapidity and extent of necrosis, providing the much needed time for resuscitation and planning the management. Intravenous immunoglobulin and hyperbaric therapy are definitely desirable [5,6,7], when indicated, but may be unnecessary if aggressive treatment protocol outlined above is adopted

Conclusion
Findings
Cunningham MW
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call