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Flashcards in Bites Deck (35):

6 factors that make bite wounds higher risk

Location: Intra oral, hands, joints, below knee
Type: puncture wounds
Cat bites > human > dogs
Delayed presentation
Patient factors: immune suppressed or elderly
Presence of peripheral vascular disease or prosthetic valve


General approach to management of bites

Anesthetize, irrigate, debride devitalized tissue
Explore in full flexion and extension for ligamentous injury
X-ray to rule out fracture or foreign body
Check blood sugar for diabetes
Consider rabies as appropriate (public health)
Close if not high risk and no signs infection
Antibiotics (iv if signs infection) if high risk
Arrange for follow up in 48 hours


7 indications for prophylactic antibiotics in bites

Cat or human
Deep puncture or extensive crush injury
Delayed presentation
Prosthetic valve
Presence of peripheral vascular disease
Intraoral, below knee, hand or joint wounds


What are the potential complications of a fight bite

Tenosynovitis, joint infection, osteomyelitis


Management of fight bite

Copious irrigation
Exploration for deeper infection, exploration for ligamentous injury
Antibiotic coverage (clavulin, or cipro/flagyl or clinda/Septra for pcn allergy)
Consider if need HIV and hep b prophylaxis if blood borne exposure


What is the bug in a cat bite

Pasteurella multocida
Presents as rapidly progressing cellulitis usually within 24 hours


Antibiotic prophylaxis for cat bites

Amox clav prophylaxis x 5 days


5 bugs associated with dog bites

P multocida
S aureus
Capnocytophaga carnimorsus


Antibiotic choice if pcn allergic in dog bites

Clinda cipro/Septra


What is the feared complication of captycytophaga canimorsus bite

Sepsis, overwhelming DIC, cutaneous gangrene at the bite site


6 diseases that can be transmitted by rodents

Rat bite fever (assoc w brain, myocardial and soft tissue abscesses ) -- streptobacillus
Hantavirus pulmonary syndrome


Appearance and toxicity of black widow spider

Yellow-red hourglass on belly
Venom is neurotoxin, release of acetylcholine and norepi at nerve terminals


Clinical presentation and treatment of black widow spider bite

Muscle cramping (back, abdomen, legs), target lesion at bite site, tachycardia hypertension, n/v, in peds can cause cardiac failure and respiratory collapse

Management: local wound care, tetanus, symptomatic treatment (benzos for cramping, opioids for pain), nitroprusside for htn
Antivenom for high risk or severe symptoms


5 Indications for antivenom in black widow bites

Children and elderly
Comorbidities (HTN, atherosclerotic disease)
Severe pain despite symptomatic treatment
Severe envenomation (seizures, uncontrolled Htn, respiratory failure)

Administer test dose of antivenom first as has horse serum (anaphylaxis will occur immediately)


Identifying feature of brown recluse spider

Brown violin shape on cephalothorax


Mechanism of toxicity of brown recluse

Venom has cytotoxic enzymes, leads to necrotic wound +\- systemic toxicity


Presentation of brown recluse bites

Initial painless bite site
Then: target lesion w pustule
3-4 d later Bullae and necrotic tissue formation w Eschar
Systemic effects: fevers, chills, n/v, hemolysis, seizures, renal failure, DIC, pulm edema


Management of brown recluse bite

Local wound care, tetanus
Supportive therapy as needed for systemic effects
Possibly dapsone (but assoc w hemolysis in g6pd and methemoglobinemia)
Delayed excision, debridement +\-skin grafting


Three types of reactions to Hymenoptera stings

Local toxic reaction
Allergic reaction
Serum sickness (7-10 days post sting)


Mechanism of toxicity in Hymenoptera stings

Local reaction to venom, in sensitized individual causes mast cell degranulation and allergic reaction
Can cause delayed type III immune response with systemic symptoms and rash (usually angioedema and urticaria)


Management of Hymenoptera stings

Local wound care, tetanus prophylaxis
Remove stingers without squeezing venom sac
Oral antihistamine
Treat anaphylaxis
Rx epi pen (60% recurrence with future exposure)


Clinical presentation of bark scorpion

Roving eye movements, muscle spasm and excessive secretions (reap distress) are hallmark,
Also causes numbness, tingling, hyperthermia,can cause cardiopulmonary arrest (mortality highest in children under 5)
Anxiety, n/v


Treatment of bark scorpion bite

Local wound care and tetanus prophylaxis
Atropine for excessive secretions
Scorpion antivenom (only available in Arizona)
Opioids and benzos for supportive treatment


Three types of Venomous marine animals



How to inactivate venom in stingers and nematocysts

Stingers immerse in hot water x 90 mins or until pain is relieved
Nematocysts immerse in acetic acid (vinegar) or isopropyl alcohol or cover in baking soda -- no fresh or tap water rinsing


Mechanism of toxicity for octopus bites

Tetrodotoxin-- causes flaccid paralysis and respiratory failure


Two major families of venomous snake bites

Viperidae (includes rattlesnakes) and elapidae


Mechanism of toxicity of viperidae bites

Venom has digestive enzymes and proteins
Local edema and toxicity (compartment syndrome, bullae, local petechia or ecchymosis)
Systemic toxicity: oral paresthesias and metallic taste, fasciculatjons, tachycardia and hypotension, anaphylaxis


Indications for antivenom or Crofab in snake bites

Severe localized pain
Moderate local edema or erythema
Spreading erythema proximally
Coagulopathy (thrombocytopenia, decreased fibrinogen, elevated PT)
Systemic symptoms
Concern for compartment syndrome


Management of verapidae bites

Immobilize in neutral, no tourniquet
Wound care, tetanus prophylaxis
Correct coagulopathy
Antivenom as indicated
Avoid fasciotomy for compartment syndrome


Presentation of elapidae envenomation

Minimal local reaction. Neurotoxin causes weakness, numbness, fasciculations, tremor, diplopia and bulbar palsies, respiratory paralysis

Antivenom in all cases


Difference between fever and hyperthermia

Fever: increased hypothalamic set point from cytokines
Hyperthermia: hypothalamus overwhelmed by heat production


Three groups of risk factors for heat illness

Increased heat production (hyperthyroid, NMS, seizure, MH)
Decreased heat loss (drugs, volume depletion, peds)
Impaired mobility (elderly, peds, alcoholic, disabled)


What is malignant hyperthermia

Genetic instability of skeletal muscles leading to excessive calcium release with exposure to anesthetic (including sux) leading to muscle rigidity and profound hyperthermia


What are heat cramps secondary to

Post exertion all secondary to relative hyponatremia with individuals repleting only with free water-- usually self limited and lab values are often normal