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| Journal of the New Zealand Medical Association,
25-June-2010, Vol 123 No 1317
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Group A streptococcal toxic shock syndrome from a
traumatic myositis
Sum Sum Lo, Anubhav Mittal, Ian Stewart
Group A streptococcal toxic shock syndrome (StrepTSS) was
defined in 1993 by the Working Group on Severe Streptococcal Infections in
response to rising cases of severe and life-threatening streptococcal infections
worldwide.1 However, streptococcal myositis
presenting as septic shock after blunt injury is
rare.2
We report StrepTSS in a previously healthy 22-year old
Caucasian male who 2 days earlier suffered a blunt injury while playing
soccer.
Case reportThe patient had seen a doctor on day 1 post-injury and was
prescribed diclofenac. He presented to the hospital on day 2 with a systolic
blood pressure (SBP) of 60 mmHg, tachycardia of 120 beats/min and tachypnoea of
28 breaths/min. He had right upper quadrant and right flank tenderness with no
bruising or external wounds. The initial impression was hypovolaemic shock
secondary to retroperitoneal haemorrhage or hepatic injury.
Computed tomography (CT) showed right-sided retroperitoneal
oedema and fractures to four right lumbar transverse processes. No solid organ
or hollow viscous injury was identified (Figure 1). Table 1 lists the
patient’s admission bloods.
Figure 1. CT scan images. Blue arrow indicates
areas of retroperitoneal oedema
 Table 1. Patient’s admission blood
results
 Despite fluid resuscitation, SBP remained at 60 mmHg. Seven
hours after admission, the patient’s temperature rose to 37.8 degrees
Celcius. His abdomen became distended but remained non-peritonitic. Due to the
history of blunt trauma, abdominal distension and septic shock, the working
diagnosis changed to septic shock secondary to small bowel injury.
Laparoscopy revealed fibrinous material in the right upper
quadrant, however the subsequent exploratory laparotomy excluded intraperitoneal
solid or viscous injury. Straw-coloured fluid from peritoneal cavity was sent
for microbiology analyses. Despite antibiotics, he deteriorated with
overwhelming sepsis leading to multiorgan failure requiring inotropes,
ventilatory support and dialysis.
The following morning, the patient’s lower abdomen and
scrotum became cellulitic. A repeat CT scan showed no definitive evidence of
necrotising fasciitis. However, to exclude a necrotising infection, the right
retroperitoneum and scrotum were explored. Extensive oedema was found in the
retroperitoneum and scrotum. Muscle and fascia were unremarkable.
Retroperitoneal fluid was sent for microbiology analyses.
Eventually, intraperitoneal and retroperitoneal fluid grew
Streptococcus pyogenes, a type of group A streptococcus.
Histologically, debrided tissue revealed acute inflammation of right psoas
muscle and scrotal wall.
With the commencement of intravenous penicillin, clindamycin
and aztreonam, the patient made a gradual recovery and was discharged from the
intensive care unit at day 9. Total hospital length of stay was 19 days.
DiscussionNon-penetrating trauma has been reported as a risk factor
for StrepTSS.3 Vimentin, a 57 kD intermediate
filament protein, has been reported to be the primary skeletal-muscle surface
protein in injured muscle which binds to group A
streptococci.4 Moderate injury increases
surface expression of vimentin.4
One to 2 days post-injury, regenerating muscle cells and
infiltrating immature muscle-cell precursors maximally express surface vimentin
facilitating the adhesion of group A
streptococci.4 Consequently, the organisms
proliferate, elaborating potent cytotoxins that cause further cell
injury.4
Maximum upregulation of surface vimentin (up to 8-fold) is
reported to occur at 48 hours after initial insult, and this correlated to our
patient’s time of presentation.5 Hamilton
et al proved that nonsteroidal anti-inflammatory drugs (NSAIDs) further enhance
binding of group A streptococci on injured
muscle.5 Our patient’s treatment with
NSAIDs for musculoskeletal pain may have contributed to the development of
StrepTSS.
Delay in making the correct diagnosis and subsequent
treatment initiation can contribute to poor outcome in
StrepTSS.2 StrepTSS has mortality rates of up
to 70% and significant morbidity from emergent amputation, extensive surgical
debridement and prolonged hospital stay.2,6
Our patient’s initial presentation with hypotension
with abdominal pain clouded the diagnosis. This case should remind clinicians
that StrepTSS should be considered in the event of blunt injury with delayed
shock (48 hours) in patients with normal haemoglobin and NSAIDs use.
Author information: Sum Sum Lo, Registrar;
Anubhav Mittal, Registrar; Ian Stewart, Consultant General and Colorectal
Surgeon; North Shore Hospital, Takapuna,
Auckland
Correspondence: Sum Sum Lo, Registrar, North Shore Hospital, Private Bag 93-503, Takapuna, North Shore City 0740, Auckland, New Zealand. Email: losumsum@gmail.com References:
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