MAMMALIAN BITES
More than 4 million animal bite wounds are sustained in
the United States each
year.
Dog Bites
Epidemiology Of all mammalian bite wounds, 80%
are inflicted by dogs,
and 15–20% of these wounds become infected.
Etiology (See Table 29-1.) In addition to
bacterial infections, dog bites
may transmit rabies (Chap. 112) and may lead to tetanus
(Chap. 100) or tularemia
(Chap. 99).
Clinical Features
• Pain, cellulitis, and a purulent, sometimes
foul-smelling discharge may develop
8–24 hafter the bite.
• Infection is usually localized, but systemic spread
(e.g., bacteremia, endocarditis,
brain abscess) can occur.
• Capnocytophaga canimorsus infection can present
as sepsis syndrome, DIC,
and renal failure, particularly in pts who are
splenectomized, have hepatic dysfunction,
or are otherwise immunosuppressed.
Cat Bites
Epidemiology In _50% of cases, infection occurs
as a result of deep tissue
penetration of narrow, sharp feline incisors. Cat bites
are more likely than dog
bites to cause septic arthritis or osteomyelitis.
Etiology The microflora is usually mixed,
although Pasteurella multocida is
the most important pathogen. Cat bites may transmit
rabies or may lead to tetanus.
Cat bites and scratches may also transmit Bartonella
henselae, the agent of catscratchdisease,
as well as Francisella tularensis, the agent of
tularemia (Chap. 99).
Clinical Features P. multocida can cause rapidly advancing, painful
inflammation
that may manifest only a few hours after the bite as well
as purulent
or serosanguineous discharge. Dissemination may occur.
Other Nonhuman Mammalian Bites
• Bite infections reflect oral flora. Bites from Old
World monkeys (Macaca
spp.) may transmit herpes B virus (Herpesvirus simiae),
which can cause CNS
infections withh ighmortality.
• Small rodents and the animals that prey on them may
transmit rat-bite fever,
caused by Streptobacillus moniliformis (in the
United States) or Spirillum minor
(in Asia). Infection with S. moniliformis manifests
3–10 days after the bite as
fever, chills, myalgias, headache, and migratory
arthralgias; these manifesta tions are followed by a maculopapular rash.
Complications can include metastatic
abscesses, endocarditis, meningitis, or pneumonia.
Diagnosis can be made
by culture on enriched media and serologic testing.
Infection with S. minor
causes local inflammation, pain, and regional
lymphadenopathy 1–4 weeks after
the bite, with evolution into a systemic illness.
Diagnosis can be made by detection
of spirochetes on microscopic examination.
Human Bites
Human bites become infected more frequently than bite
wounds from other
animals. Occlusional injuries are inflicted by
actual biting. Clenched-fist injuries
result when the fist of one individual strikes the teeth
of another. These injuries
are particularly prone to serious infection.
Etiology See Table 29-1.
TREATMENT
• Wound management: Wound closure is controversial
in bite injuries. After
thorough cleansing, facial wounds are usually sutured for
cosmetic reasons
and because the abundant facial blood supply lessens the
risk of infection.
For wounds elsewhere on the body, many authorities do not
attempt primary
closure, preferring instead to irrigate the wound
copiously, debride devitalized
tissue, remove foreign bodies, and approximate the
margins. Delayed primary
closure may be undertaken after the risk of infection has
passed.
• Antibiotic therapy: See Table 29-1.
• Tetanus: A booster for pts immunized previously
but not boosted within
5 years should be considered, as should primary
immunization and tetanus
immune globulin administration for pts not previously
immunized.
VENOMOUS SNAKEBITES
Etiology and Epidemiology Worldwide, at least 30,000 to 40,000
people
die eachyear from venomous snakebite injuries, most often
in temperate and
tropical regions. The overall mortality rate for venomous
snakebite is _1%
among U.S. victims who receive antivenom. Eastern and
western diamondback
rattlesnakes are responsible for most deaths from snakebite
in the United States.
Snake venoms are complex mixtures of enzymes and other
substances that promote
vascular leaking and bleeding, tissue necrosis, and
neurotoxicity and affect
the coagulation cascade.
TREATMENT
Field Management
• Get the victim to definitive care as soon as possible.
• Keep the victim inactive to minimize systemic spread of
venom.
• If the victim is _60 min from medical care, a proximal
lymphatic-occlusive
constriction band may limit the spread of venom but
should be applied
so as not to interfere witharterial flow.
• Splint a bitten extremity and keep it at heart level.
• Avoid incisions into the bite wound, cooling,
consumption of alcoholic
beverages by the victim, and electric shock.
Hospital Management
• Monitor vital signs, cardiac rhythm, and O2 saturation
closely.
• Note the level of erythema and swelling and the limb
circumference every
15 min until swelling has stabilized.
Treat shock initially with crystalloid fluid
resuscitation (normal saline or
Ringer’s lactate). If hypotension persists, try 5%
albumin and vasopressors.
• Begin the search for appropriate, specific antivenom
early in all cases of
known venomous snakebite, regardless of symptoms. In the
United States,
round-the-clock assistance is available from the
University of Arizona Poison
and Drug Information Center (520-626-6016).
1. Rapidly progressive and severe local findings or
manifestations of
systemic toxicity (signs and symptoms or laboratory
abnormalities)
are indications for IV antivenom.
2. Most antivenoms are of equine origin and carry risks
of anaphylactic,
anaphylactoid, or delayed-hypersensitivity reactions. The
newest antivenom
available in the United States for pit viper bites
reduces this
risk.
3. Pts should be premedicated with IV antihistamines
(e.g., diphenhydramine,
1 mg/kg up to a maximum dose of 100 mg; plus cimetidine,
5–10 mg/kg up to a maximum dose of 300 mg) and given IV
crystalloids
to expand intravascular volume. Epinephrine should be
immediately
available. The antivenom should be administered slowly in
dilute solution witha physician present in case of an
acute reaction.
• Elevate the bitten extremity only when antivenom is
available.
• Update tetanus immunization.
• Observe pts with signs of envenomation in the hospital
for at least 24 h.
Pts with “dry” bites should be watched for at least 8 h
because symptoms are
commonly delayed.
MARINE ENVENOMATIONS
Invertebrates
Injuries from nematocysts (stinging cells) of hydroids,
fire coral, jellyfish, Portuguese
man-of-war, and sea anemones cause similar clinical
symptoms that
differ in severity.
Clinical Features Pain (prickling, burning, and
throbbing), pruritus, and
paresthesia develop immediately at the site of the bite.
Neurologic, GI, renal,
cardiovascular, respiratory, rheumatologic, and ocular
symptoms have been described.
TREATMENT
• Decontaminate the skin immediately with vinegar (5%
acetic acid) or rubbing
alcohol (40–70% isopropanol). Baking soda, unseasoned
meat tenderizer
(papain), or lemon or lime juice may be effective.
• Shaving the skin may help remove nematocysts.
• After decontamination, topical anesthetics,
antihistamines, or steroid lotions
may be helpful.
• Narcotics may be necessary for persistent pain.
• Muscle spasms may respond to IV 10% calcium gluconate
(5–10 mL) or
diazepam (2–5 mg titrated upward as needed).
Vertebrates
Marine vertebrates, including stingrays, scorpionfish,
and catfish, are capable
of envenomating humans.
Clinical Features
• Immediate and intense pain at the site can last up to 48 h.
Systemic symptoms include weakness, diaphoresis, nausea,
vomiting, diarrhea,
dysrhythmia, syncope, hypotension, muscle cramps, muscle
fasciculations,
and paralysis. Fatal cases are rare.
• Stingray wounds can become ischemic and heal poorly.
• The sting of a stonefish is the most serious marine
vertebrate envenomation
and can be life-threatening.
TREATMENT
• Immerse the affected part immediately in nonscalding
hot water (113_F/
45_C) for 30–90 min.
• Explore, debride, and vigorously irrigate the wound.
• Antivenom is available for stonefishand scorpionfish
envenomations.
• Leave wounds to heal by secondary intention or to be
treated by delayed
primary closure.
• Update tetanus immunization.
• Consider empirical antibiotics to cover Staphylococcus
and Streptococcus
spp. for serious wounds or envenomations in
immunocompromised hosts.
Sources of Antivenoms and Other
Assistance
Antivenom for stonefishand severe
scorpionfishenvenomation is available
in the United States through the pharmacies of Sharp
Cabrillo Hospital Emergency
Department, San Diego, CA (619-221-3429) and Community
Hospital
of Monterey Peninsula (CHOMP) Emergency Department,
Monterey, CA
(408-625-4900). Divers Alert Network is a source of
helpful information
MARINE POISONINGS
Ciguatera
Ciguatera poisoning is the most common nonbacterial food
poisoning associated
withfishin the United States. Tropical and semitropical
marine coral reef fish
are usually the source; 75% of cases involve barracuda,
snapper, jack, or grouper.
Toxins may not affect the appearance or taste of the fish
and are resistant
to heat, cold, freeze-drying, and gastric acid.
Clinical Features Most victims experience diarrhea,
vomiting, and abdominal
pain 3–6 hafter ingestion of contaminated fish and
develop myriad
symptoms within 12 h, including neurologic signs (e.g.,
paresthesia, weakness,
fasciculations, ataxia), maculopapular or vesicular rash,
and hemodynamic instability.
A pathognomonic symptom—reversal of hot and cold
perception—
develops within 3–5 days and can last for months. Death
is rare. A diagnosis
is made on clinical grounds.
TREATMENT
Therapy is supportive and based on symptoms. Cool showers,
hydroxyzine
(25 mg PO q6–8h), or amitriptyline (25 mg PO bid) may
ameliorate pruritus
and dysesthesias. During recovery, the pt should avoid
ingestion of fish, shellfish,
fish oils, fish or shellfish sauces, alcohol, nuts, and
nut oils.
Paralytic Shellfish Poisoning (PSP)
PSP is induced by ingestion of contaminated clams,
oysters, scallops, mussels,
and other species that concentrate water-soluble, heat-
and acid-stable chemical
toxins. Pts develop oral paresthesias that progress to
the neck and extremities
and that change to numbness within minutes to hours after
ingestion of contam inated shellfish. Flaccid paralysis and respiratory
insufficiency may follow 2–
12 h later. Treatment is supportive. If pts present
within hours of ingestion,
gastric lavage and stomachirrigation with 2 L of a 2%
sodium bicarbonate
solution may help. The pt should be monitored for
respiratory paralysis for at
least 24 h.
Scombroid
Etiology and Clinical Features Scombroid poisoning is a histamine
intoxication
due to inadequately preserved or refrigerated scombroid
fish(e.g.,
tuna, mackerel, saury, needlefish, wahoo, skipjack, and
bonito); it can also occur
with exposure to nonscombroid fish, including sardines
and herring. Within 15–
90 min of ingestion, victims present withflush ing,
pruritus or urticaria, bronchospasm,
GI symptoms, tachycardia, and hypotension. Symptoms
generally
resolve within 8–12 h.
TREATMENT
Treatment consists of antihistamine (H1 or H2)
administration.
Pfiesteria Poisoning
Etiology and Clinical Features Pfiesteria, a dinoflagellate identified in
Maryland waters, releases a neurotoxin that kills fish
within minutes. In people,
exposure to Pfiesteria can cause a syndrome
defined by the CDC as either of
two groups of signs or symptoms: (1) memory
loss/confusion or acute skin
burning on contact with infested water; or (2) at least
three of the following:
headache, rash, eye irritation, upper respiratory
irritation, muscle cramps, and
GI symptoms. Neurocognitive defects improve within 3–6
months after cessation
of exposure.
TREATMENT
Milk of magnesia (1 tsp qd) followed by cholestyramine (1
scoop in 8 oz
water qid) for 2 weeks has been a successful remedy in
some cases.
ARTHROPOD BITES AND STINGS
Spider Bites
RECLUSE SPIDER BITES Severe necrosis of skin and SC
tissue follows
a bite by the brown recluse spider. The spider is 7–15 mm
in body length,
has a 2- to 4-cm leg span, and has a dark violin-shaped
spot on its dorsal surface.
Spiders seek dark, undisturbed spots and bite only if
threatened or pressed
against the skin. The venoms contain enzymes that produce
necrosis and hemolysis.
Clinical Features
• Initially the bite is painless or stings, but within
hours the site becomes
painful, pruritic, and indurated, with zones of ischemia
and erythema.
• Fever and other nonspecific systemic symptoms may
develop within 3 days
of the bite.
• Lesions typically resolve within 2–3 days, but severe
cases can leave a large
ulcer and a depressed scar that take months to years to
heal. Deaths are rare and
are due to hemolysis and renal failure.
TREATMENT
• Wound care, cold compress application, elevation and
loose immobilization
of the affected limb, and administration of analgesics,
antihistamines,
antibiotics, and tetanus prophylaxis should be undertaken
as indicated.
• Dapsone administration within 48–72 h (50–100 mg PO bid
after G6PD
deficiency has been ruled out) may halt progression of
necrotic lesions.
WIDOW SPIDER BITES Etiology and
Clinical Features The black
widow spider is found in every U.S. state except Alaska
but is most abundant
in the Southeast. It measures up to 1 cm in body length
and 5 cm in leg span,
is shiny black, and has a red hourglass marking on the
ventral abdomen. Female
widow spiders produce a potent neurotoxin that binds
irreversibly to nerves and
causes release and depletion of acetylcholine and other
neurotransmitters from
presynaptic terminals. Within 30–60 min, painful cramps
spread from the bite
site to large muscles of the extremities and trunk.
Extreme abdominal muscular
rigidity and pain may mimic peritonitis, but the abdomen
is nontender. Other
features include salivation, diaphoresis, vomiting,
hypertension, tachycardia,
and myriad neurologic signs. Respiratory arrest, cerebral
hemorrhage, or cardiac
failure may occur.
TREATMENT
Treatment consists of local cleansing of the wound,
application of ice packs
to slow the spread of the venom, and tetanus prophylaxis.
Analgesics, antispasmodics,
and other supportive care should be given. Equine
antivenom is
available; rapid IV administration of 1 or 2 vials
relieves pain and can be lifesaving.
However, antivenom use should be reserved for severe
cases involving
respiratory arrest, refractory hypertension, seizures, or
pregnancy because of
anaphylaxis risk and serum sickness.
Scorpion Stings
Etiology and Clinical Features Among the venoms of scorpions in the
United States, only the venom of the bark scorpion (Centruroides
sculpturatus
or C. exilicauda) is potentially lethal. The bark
scorpion is yellow-brown and
7 cm long and is found in the southwestern United States
and northern Mexico.
Its neurotoxin opens sodium channels, and neurons fire
repetitively. The sting
causes little swelling, but pain, paresthesia, and
hyperesthesia are prominent.
Cranial nerve dysfunction and skeletal muscle
hyperexcitability develop within
hours. Symptoms include restlessness, blurred vision,
abnormal eye movements,
profuse salivation, slurred speech, diaphoresis, nausea,
and vomiting. Complications include tachycardia, arrhythmias, hypertension,
hyperthermia, rhabdomyolysis, and acidosis. Manifestations peak at 5 hand
subside within a day or two, although paresthesias can last for weeks.
TREATMENT
Aggressive supportive care should include pressure
dressings and cold packs
to decrease the absorption of venom. Continuous IV
administration of midazolam
to decrease agitation and involuntary muscle movements
may be
needed. The benefit of scorpion antivenom has not been
established in controlled
trials.
Hymenoptera Stings
The hymenoptera include apids (bees and bumblebees),
vespids (wasps, hornets,
and yellow jackets), and ants. About 50 deaths from
hymenoptera stings occur
annually in the United States, nearly all due to allergic
reactions to venoms.
Clinical Features
• Honeybees can sting only once; other bees, vespids, and
ants can sting many
times in succession.
• Uncomplicated stings cause pain, a wheal-and-flare
reaction, and local
edema that subsides within hours.
• Multiple stings can lead to vomiting, diarrhea, generalized
edema, dyspnea,
hypotension, rhabdomyolysis, renal failure, and death.
• Large (_10-cm) local reactions progressing over 1–2
days are not uncommon
and resemble cellulitis but are hypersensitivity
reactions.
• About 0.4–4% of the U.S. population exhibits
immediate-type hypersensitivity
to insect stings. Serious reactions occur within 10 min
of the sting and
include upper airway edema, bronchospasm, hypotension,
shock, and death.
TREATMENT
• Stingers embedded in skin should be removed promptly by
any method.
• The site should be cleansed and ice packs applied.
Elevation of the bite
site and administration of analgesics, oral
antihistamines, and topical calamine
lotion may ease symptoms.
• Oral glucocorticoids are indicated for large local
reactions.
• Anaphylaxis is treated with epinephrine hydrochloride
(0.3–0.5 mL of a
1:1000 solution, given SC q20–30min as needed). For
profound shock, epinephrine
(2–5 mL of a 1:10,000 solution by slow IV push) is
indicated. Pts
should be observed for 24 h because of the risk of
recurrence.
• Pts with a history of allergy to insect stings should
carry a sting kit and
seek medical attention immediately after the kit is used.
Adults with a history
of anaphylaxis should undergo desensitization.
Tick Bites and Tick Paralysis
Etiology and Clinical Features
• Ticks are important carriers of vector-borne diseases
in the United States.
• Ticks attach and feed painlessly on blood from their
hosts, but tick secretions
may produce local reactions. Tick bites may cause a small
area of induration
and erythema. A necrotic ulcer occasionally develops;
chronic nodules or tick
granulomata may require surgical excision. Tick-induced
fever and malaise resolve
24–36 hafter tick removal.
• Tick paralysis is an ascending flaccid paralysis due to
a toxin in tick saliva
that causes neuromuscular block and decreased nerve
conduction. Paralysis begins
in the lower extremities 5–6 days after the tick’s
attachment and ascends
symmetrically, causing complete paralysis of the
extremities and cranial nerves.
Deep tendon reflexes are decreased or absent, but sensory
examination and LP
yield normal findings. Tick removal results in
improvement within hours. Failure
to remove the tick may lead ultimately to respiratory
paralysis and death.
The tick is usually found on the scalp.
TREATMENT
Ticks should be removed with forceps applied close to the
point of attachment,
and the site of attachment should then be disinfected.
Removal within 48 h of attachment usually prevents transmission of the agents
of Lyme disease,
babesiosis, and ehrlichiosis. Protective clothing and
DEET application are
protective measures that can be effective against ticks.
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