4
bugs,
biting
flies,
superficial
skin
infections,
diabetic ulcers, plant puncture wounds, sporotrichosis,
toxic
epidermal
necrolysis,
pyoderma
gangrenosum, erythema nodosum, erythema chronicum
migrans, Herpes zoster, Herpes simplex, erythema multiforme, purpura fulminans, contact dermatitis,
etc.
- brown spider venoms are immunologically distinct, but have similar toxic effects - cytotoxic and
hemolytic component responsible for these effects is probably sphingomyelinase D
- activation of the complement cascade induces a series of autopharmacologic changes in the victim
that
amplify
injury
- cutaneous changes initiated by venom-induced endothelial damage in small dermal vessels ->
become occluded with microthrombi -> leads to vascular stasis and infarction -> PMNs are attracted
to the site by chemotaxis -> propagate inflammation & necrosis
2.
Clinical Manifestations:
- extremely rare for the victim to see the offending spider (relatively painless bite and large percentage
of bites occur while the victim is asleep)
- severity varies from mild, temporary irritation at the bite site to severe, potentially fatal systemic
poisoning
- first several hrs: pruritus, tingling, mild swelling, & redness or
blanching at the site
- variable degrees of pain & tenderness due to local vasospasm and ischemia within 2-8 hr
- within 12-18 hr, a small, central vesicle (clear or hemorrhagic) often develops at the site and is
surrounded by an irregular zone of erythema or ecchymosis and edema
- bleb soon ruptures and erythema changes to violaceous discoloration
- 5-7 d, the bite site undergoes aseptic necrosis, the center becomes depressed below the normal level
of the skin ("volcano lesion"), and a black eschar forms -> later sloughs, leaving an open ulcer that
heals over weeks to months
- bites to fatty regions (buttocks, thighs, abdomen, etc.) tend to be more severe
- rarely does necrosis involve deep structures such as nerves, muscles, tendons, or ligaments
- lesions destined to develop significant necrosis usually demonstrate early evidence of local ischemia
-
"systemic
(viscerocutaneous)
loxoscelism"
is rare, but may be rapidly progressive and severe,
particularly
in
children
-
systemic
symptoms
start 24-72 hr after the bite (occasionally before
cutaneous findings become impressive); often flu-like with fever, chills, headache, malaise, weakness,
nausea,
vomiting,
myalgias,
arthralgias;
hemolytic anemia with hemoglobinemia, hemoglobinuria,
jaundice,
thrombocytopenia,
disseminated
intravascular coagulation, acute renal failure, shock,
seizures, and coma have been reported
- severity of systemic symptoms does not correlate with severity of cutaneous changes
3.
Management:
a. Field Management:
-
ice
application
b. Hospital Management:
i. Dermonecrosis:
- differential diagnosis may be difficult (don't overdiagnose "brown recluse bite"!)
- laboratory evaluation: complete blood count (including platelets) & urinalysis; if any evidence of
consumptive coagulopathy, hemolysis, or hemoglobinuria, get PT/PTT, electrolytes, BUN, Cr,
blood sugar, liver function tests, serum haptoglobin and a type and cross-match
- follow daily blood counts and UA's for approximately 3 days in patients with significant lesions
even
if
not
admitted
- more frequent labs if manifestations of systemic poisoning
-
currently
no
clinically
available
laboratory method of making the diagnosis early (an in vitro
lymphocyte
transformation
test
can confirm envenomation at 6 wk after bite)
-
controversy
exists
over
proper management of necrotic lesions:
- majority require only local wound care (cleansing of the bite site, application of a sterile
dressing,
immobilization
with
a
well-padded splint, and tetanus prophylaxis as necessary)
- local application of ice for 72 hr to reduce sphingomyelinase activity
