Bites Flashcards
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
Tetanus
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 Immunesuppression 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 Fusobacterium Bacteroides 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 Plague Hantavirus pulmonary syndrome Leptospirosis Tularaemia Sporotrichosis
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
Pregnancy
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
Stingers
Nematocysts
Bites
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
