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antivenom against any Platyceps spp. Also, from information in the presenting history,
there is no basis to contemplate antivenom administration even if it was available.
Shortly after the aforementioned treatments were initiated, the patient developed
generalized muscle aches and hyperpyrexia that were attributed to wound site infec-
tion. The patient improved, was discharged, then gradually exhibited body aches
as well as severe stiffness of the back, upper arms, and neck. She was re-admitted
20 days after the initial episode and on admission persistent stiffness with muscle
spasm and hyper-reflexia were noted (Chroni et al., 2005). Although laboratory tests
were within normal limits, needle electromyography of affected muscles showed sus-
tained motor unit activity with reduction induced by i.v. diazepam. The authors then
treated the patient for suspected tetanus with antitetanus immunoglobulin, antibiotics,
and diazepam (Chroni et al., 2005). Shortly thereafter (2 months after the initial admis-
sion), the patient developed flaccid paraparesis. A nerve conduction study indicated the
presence of axonal motor neuropathy. A cerebral spinal fluid (CSF) analysis was acel-
lular, but with markedly elevated protein (110 mg/dL; Chroni et al., 2005). There was
no evidence of neuromuscular junction failure, and a tentative diagnosis of Guillain-
Barré syndrome (GBS) was considered. The patient was treated with i.v. administra-
tion of immunoglobulin, resulting in mild improvement. However, over the following
month, the patient developed quadriplegia without cranial nerve involvement and with
intact sensation. Magnetic resonance imaging, autoimmune screening, and comprehen-
sive blood tests were all negative (Chroni et al., 2005).
The patient was given a course of 60 mg of prednisone/day and was discharged
tetraplegic. She was again re-admitted 1 month later and deteriorated during this
admission. The patient expired 5.5 months after the alleged P. najadum bite; death
was ascribed to massive mesenteric thrombosis (Chroni et al., 2005).
The authors stated that the case was inconsistent with tetanus (due to a lack of
trismus and facial muscle involvement as well as the progressive autonomic domi-
nant neuropathy) or GBS (due to the irreversible progression to quadriplegia and
fatal outcome; Chroni et al., 2005). The results of numerous tests were not consistent
with myasthenia, myasthenic syndrome, or polymyositis (Chroni et al., 2005). They
also considered that administration of tetanus toxoid may have caused a polyradicu-
litis, although previously documented cases have usually involved multiple doses and
this patient received only a single dose (Chroni et al., 2005; Reinstein et al., 1982).
However, while considering the aforementioned likely etiologies, the authors sug-
gested that this complex and unfortunate case might be due to “ an immune reaction
against neural antigens generated by the snake toxins.” This was hypothesized to have
caused a widespread inflammatory disease in the nerve roots (Chroni et al., 2005).
These complex polyneuropathies often are a diagnostic and management chal-
lenge. Their features, natural history, diagnosis, and management are far too exten-
sive to discuss here and have been thoroughly reviewed (Goetz, 2007; Longmore
et al., 2001). Some of these neuropathies can be associated with comorbidities, but
the authors asserted an unremarkable medical history of their patient (Chroni et al.,
2005). The possibility of GBS can be briefly considered, as it is often associated with
a recent history (usually within weeks) of infection [e.g., viral upper respiratory infec-
tion, atypical pneumonia (e.g., Mycoplasma pneumoniae ), herpes zoster reactivation,
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