Matthew P Soape MDa, Deephak Swaminath MDa, Mark Whealy MDb, Vipul Desai MDc
Correspondence to Matthew Soape MD. Email: matthew.soape@ttuhsc.edu
SWRCCC 2014;2(6):45-48
doi: 10.12746/swrccc2014.0206.076
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Systemic loxoscelism is a rare complication from the bite of spiders in the genus. These bites usually cause painful indurated skin reactions, including necrosis, and occasionally cause systemic complications, such as rhabdomyolysis, acute renal failure, and disseminated intravascular coagulation. Our case had multiple systemic complications, including bilateral globus pallidus infarcts with right arm weakness.
Keywords: spider bite, Loxosceles reclusa, systemic loxoscelism
...................................................................................................................................................................................................................................................................................................................................Rhabdomyolysis, acute renal failure, and disseminated
intravascular coagulation (DIC) frequently
occurs in patients with severe systemic loxoscelism.1 The case presented here had these complications
plus acute respiratory failure and bilateral globus pallidus
lesions. A literature search failed to recover any
cases that reported central nervous system (CNS) lesions
associated with systemic loxoscelism. In this article,
we discuss the pathophysiology underlying systemic
loxoscelism that probably explains the ischemic
injury to the CNS.
A 47-year-old Caucasian man was found unresponsive
in Carlsbad, NM, was unable to protect
his airways, and was intubated at the scene. In the
ER, the patient had a temperature of 100.9 °F, a BP
of 173/104 mmHg, and a pulse rate of 117 beats per minute. He had swelling and erythema on the parieto-
occipital aspect of his head. He had diffuse crackles
in both lungs.His CBC included WBC 9.4 k/μL,
Hb 15.7 gm/dl, Hct 45.2 %, and platelet 92 k/μL. His
labs showed evidence of rhabdomyolysis (CK 57,125
IU/L), acute renal failure (BUN 37 mg/dL; Cr 4.1 mg/
dL), hepatitis (ALT 5,721 intl units/L; AST 12,831 intl
units/L), and coagulopathy (PT 20.9 sec; INR 2.02;
PTT 35.5 sec, D-Dimer 11,313 ng/ml). He also had a
high LDH (5,372 units/L) and developed a mild anemia
during his hospitalization (Hb 15.7 gm/dl on admission
with a decrease to 11.8 gm/dl on hospital day
six associated with an increase in bilirubin from 0.8
mg/dl on admission to 1.3 mg/dl day four). During the
first 24 hours of admission, a necrotic lesion formed
at the site of the swelling on his head (Figure 1). This
lesion had a raised edge with surrounding erythema
and grew to a circumference of 5 cm. The dermatology
consult concluded the lesion was most likely secondary
to a spider bite. No information regarding any
spider bite or sighting could be obtained. The patient
was successfully extubated and transferred to floor
status after day three.
On day five, he noticed weakness of his right
upper extremity (RUE). A CT scan of his head showed
a subacute infarct in the internal capsule, and a subsequent
MRI demonstrated infarcts in both globus
pallidi (Figure 2). The patient continued to spike fevers
throughout his hospitalization. On day 10 of hospitalization,
the patient had a large indurated area on
his right lateral thigh. An Infectious Disease consult
recommended starting vancomycin for cellulitis. All of
his labs and symptoms, including his RUE weakness,
improved throughout his remaining hospital stay.
He was discharged home on day 12 of hospitalization
with instructions to continue vancomycin for two
weeks.
Figure1: Photographs of the site of suspected brown recluse envenomation on the second day of admission (left) and 10 days later (right).
Figure 2: MRI head of our patient on day four of admission after complaining of right upper extremity weakness. a) Diffusion weighted imaging showing bilateral globus pallidus hyperintensities which correlate with hypointensities seen on the b) diffusion coefficient image c) T2 FLAIR d) coronal T2 images. Yellow arrows pointing to bilateral globus pallidus hyperintesities.
Systemic loxoscelism is a rare complication
from the bite from spiders in the genus Loxosceles.1
These bites usually cause painful indurated skin reactions
but can cause necrosis and ulcers. Necrotic
ulcers may take months to heal and require debridement
and skin grafting. Some patients develop systemic
signs and symptoms, including mild fever, myalgias,
arthralgias, rhabdomyolysis, hemolytic anemia, DIC, and acute renal failure, and have very complicated
hospital courses.1 The brown recluse spider
(Loxosceles reclusa) is frequently responsible for these
bites in the southern United States.
This patient presented with erythematous
swelling on his scalp that progressed to a large area
of necrosis consistent with a brown recluse spider
bite. Although we cannot be certain that this was
a spider bite, it is strongly suspected based on the
available information, the clinical course, and the fact
that the brown recluse is endemic to the area where
the incident occurred. The lack of confirmation is not
unusual, and in the nine case reports with 16 patients
there were only two confirmed brown recluse
spider bites (the spider was captured and brought in
for identification) and two sightings.2-10 None of these
cases had CNS involvement. The most common severe
reactions to a Loxosceles bite in these case reports
were hemolysis, rhabdomyolysis, acute kidney
injury, and death. Since this diagnosis is often one of
exclusion, a thorough differential diagnoses is always
needed. Other causes for rhabdomyolysis, including
recreational drug use and statin therapy, seemed unlikely.
The patient had a negative urine drug screen
and had only started statin therapy a few days prior to
hospitalization. He had no history of anemia and hereditary
causes of hemolysis were unlikely given his
age. Sepsis could explain his DIC, but blood cultures
taken on admission were negative at the time when
the coagulopathy and thrombocytopenia were at their
worst lab values. A separate blood culture on day
five grew Staphylococcus epidermidis, a common skin
bacterium which could have been introduced secondary
to his spider bite. Also DIC occurs more frequently
in Gram negative sepsis than Gram positive sepsis.
Cancer and trauma were also ruled out.
This case demonstrates the possibility of
CNS injury can occur in systemic loxoscelism. This
patient’s infarcts could reflect hypoxia from the acute
respiratory failure or a direct effect of venom toxins
on the CNS circulation. If the CNS infarcts were secondary
to hypoxia, the CNS involvement should have
been more diffuse with laminar cortical necrosis and
not just localized to the globus pallidus. Carbon monoxide
poisoning can cause diffuse cerebral injury, but
his daughter who was sleeping in the same room had
no adverse effects. The ischemic injury was probably
secondary to microvascular thrombosis secondary to
DIC. A possible mechanism is the induction of a hypercoagulable
state by the 35 kD sphingomyelinase
D in Loxosceles venom. This protein cleaves thrombomodulin
and endothelial protein C receptor through
the activation of an endogenous metalloproteinase.
These cells can not normally express surface proteins
to aid in the thrombin induced activation of protein C,
and this process could cause DIC and thrombosis.11
Also, Loxosceles venom has direct cytotoxic effects
on the endothelial cells which produce morphological
changes and detachment from the subendothelial
layer.12 This would expose the subendothelial collagen
leading to binding of von Willebrand factor and
subsequent platelet activation and thrombosis. Consequently,
the combination of vascular injury and DIC
with fibrin deposition causes tissue ischemia and
injury. The localization to the globus pallidi is unexplained.
In conclusion, this case has a unique presentation
of systemic loxoscelism. He had common
features, such as hemolysis, acute kidney injury, and
rhabdomyolysis, and unique infarcts in the basal ganglia.
This finding has not been reported in the literature
to date.
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