Dermatologic Disorders
Bites and Stings
Conni Nevills
Bites: Mammalian
Background
Dog bites are responsible for >3 to 4 million emergency department (ED) visits annually.
One third to one half of these bites occur in children, with higher incidence in males.
Children are more likely to sustain disfiguring facial bites than adults.
Definition
Wound inflicted by a person or animal that disrupts the epidermal layer of skin.
Etiology/Types
Dog and human bites are the most common types of bites.
Clinical Presentation
Bleeding, pain, disfigurement, erythema, edema, exposed subcutaneous tissue.
Diagnostic Evaluation
Radiographic evaluation if suspected bone fracture or pene-trating wound over bone/joint or to evaluate for foreign body inoculation.
Wound culture if appears infected.
Management
Thorough wound debridement and irrigation; copious amounts of volume with high-pressure syringe irrigation.
No consensus exists on primary wound closure.
Antimicrobial therapy indicated for:
Moderate or severe bite wounds and puncture wounds.
Facial bites, hand or foot, or genital-area wounds.
Immunocompromised or asplenic host.
Signs of wound infection.
Evaluate for risk of rabies (dog, cat bites) and for human immunodeficiency virus (human bites).
Evaluate tetanus vaccination status; may require booster.
No prophylaxis is required for new wounds with simple epidermal injury (e.g., scratches and abrasions).
Antimicrobial Agent Recommendations (See Table 21.1).
Follow-Up
Evaluation for signs of infection in 48 hours.
PEARLS
Provide coverage for methicillin-resistant Staphylococcus aureus in severe bite wounds.
Ampicillin-clavulanate monotherapy does not provide coverage for methicill in-resistant Staph. aureus.
All pediatric bite wounds require evaluation.
Bites: Snakes
Background
Several thousand snake bites occur yearly in the United States.
Mortality is rare due to advances in therapy.
Identification of snake species is important; majority of snakes are nonvenomous.
Historical clues include geographic location (e.g., woodlands, water, desert), presence of rattlers, and length.
Definition
Envenomation occurs when venom is released through hollow fangs into the dermal layer of skin releasing a mixture of cytotoxic, hemolytic, and neurotoxic polypeptides.
The substances damage local endothelium and can trigger systemic envenomation due to increased permeability which perpetuates the envenomation.
Etiology/Types
Venomous species include rattlesnakes, cottonmouth moccasins, copperheads, and coral snakes.
TABLE 21.1 Antimicrobial Agent Recommendations for Dog, Cat, and Human Bites | ||||||||||||
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Clinical Presentation
Puncture marks (may be absent in some species), edema, erythema, discoloration and development of bullae, pain.
Signs of systemic toxicity include cardiovascular, respiratory, renal, and neurologic symptoms, but these are rare.
Diagnostic Evaluation
Laboratory evaluation: hemoglobin/hematocrit, platelets, serum creatinine, alanine transaminase (ALT) and aspartate aminotransferase (AST), prothrombin time, fibrinogen, and creatine kinase.
Management
Initial first aid is to cleanse wound site with soap and water and immobilize extremity, placing it at the level of the heart.
Consultation with poison control and expert providers experienced in managing snake bites (if available).
Antivenom administration if anaphylaxis, respiratory distress, hemolytic abnormalities, uncontrolled hypertension, or extreme pain.
Pain control with narcotics if indicated.
Frequent evaluation with measurements of affected tissue.
Antibiotics are not indicated unless direct evidence of bacterial pathogen.
Evaluate tetanus status; administer tetanus vaccination if needed.
Bites: Spider
Background
Two species of spiders have venom that causes clinically significant illness in North America: the brown recluse (Loxosceles reclusa) and the black widow (Latrodectus mactans).
Definition
Brown recluse venom triggers the inflammatory cascade; can develop into tissue necrosis.
Black widow venom causes acute onset of intense pain via catecholamine release affecting neurotransmitters.
Etiology/Types
A black widow bite may present with fang marks or target sign.
Clinical Presentation
Brown recluse.
Pain at the site of the bite.
A ring of white tissue ischemia may develop, followed by a blister or pustule, and then a bull’s-eye appearance.
Local symptoms typically begin 3 to 4 hours after the bite.
Severe envenomation occurs 24 to 72 hours after bite and presents with fever, chills, nausea, vomiting, signs of kidney injury, and alterations in hemolytic composition and function.
May lead to thrombocytopenia, hemolysis, shock, kidney failure, bleeding, or pulmonary edema.
Mortality is typically a result of respiratory failure or severe intravascular hemolysis.
Black widow.
Sudden onset of acute pain, swelling, muscle spasms, tachycardia, hypertension, pain, and agitation.
May have positive “tap test” (i.e., tapping at the suspected site of the bite elicits pain).
Increased intracranial pressure, significant hypertension, and respiratory failure are the most serious potential reactions.
Diagnostic Evaluation
Brown recluse.
No specific laboratory test. Complete blood count (CBC), basic metabolic profile, AST and ALT, coagulation studies, urinalysis (may provide signs of systemic disease; hemoglobinuria and/or myoglobinuria).
Black widow.
CBC, metabolic panel, coagulation studies, ECG, and urinalysis.
Management
Brown recluse.
Based on clinical and diagnostic findings.
Local debridement, elevation, loose immobilization, and cool compresses.
Avoid strenuous activity; may spread venom.
Antivenom rarely indicated and carries significant adverse effects.
Patients with evidence of systemic illness require hospitalization for evaluation of coagulopathy, hemolysis, and renal failure.
No antivenom available in the United States for brown recluse spider.
Black widow.
Local wound care, tetanus prophylaxis, pain control, cool compresses/ice packs.
Treat symptoms of infection with broad-spectrum antibiotics.
Antivenom is considered in severe cases; associated with significant risk for anaphylaxis and in children <40 kg and pregnant women.
Mild cases: monitor for 6 hours. If progressive/worsening symptoms, hospital admission is indicated.
Treat hypertension aggressively.
Muscle cramps can be treated with benzodiazepines, opioids, or dantrolene.
Both brown recluse and black widow.
Consultation with providers/specialists experienced in spider bites.
PEARLS
Brown recluse spider bite presentation can be similar to an early community-acquired Staph. aureus infection or other spider bite.
Black widow antivenom derived from horse serum; skin testing recommended prior to administration; evaluates for hypersensitivity.
Mortality with black widow bites is approximately 5%, though significantly higher in young children (50%).
Stings: Bees and Wasps
Background
Possess stingers; release venom resulting in local reaction or anaphylaxis in some patients.
Wasps are differentiated from bees by their smooth bodies and stingers which they can retract; ability to sting multiple times.
Bee stingers are barbed which causes their demise after stinging.
Account for most deaths associated with envenomation; 50% of deaths occur within 30 minutes of sting; 75% within 4 hours.
Fatal reactions can occur with the generalized reaction to a sting; however, more commonly follows a previous sting that was associated with more mild generalized reaction. Shorter interval between stings increases likelihood of severe reaction.
Pathophysiology
Venom contains enzymes, vasoactive chemicals, and peptides that cause catecholamine release, mast cell degranulation, and pain.
Edema is a result of increases in cell membrane permeability.
Triggers strong immune response, specifically mast cells (i.e., anaphylaxis) in some individuals.
Etiology/Types
A local reaction is contained in the dermal layer of tissue and is a self-limiting condition.
Systemic reactions occur as a result of massive IgE-mediated hypersensitivity reaction to envenomation.
Clinical Presentation
Factors that influence the clinical presentation include the amount of injected venom, the number of stings, and the host’s immune response.
Local reactions are characterized by pain, erythema, pruritus, warmth, and mild edema.
Symptoms of systemic illness include nausea, vomiting, abdominal pain, urticaria, and evidence of renal injury.
Diagnostic Evaluation
Laboratory evaluation: CBC, complete metabolic profile, coagulation studies, creatine kinase.
If concern for systemic involvement, consider cardiac biomarkers (predisposition for myocardial infarction), chest radiograph for pulmonary edema, and ECG to evaluate for ST segment changes.
Management
Remove stingers, if possible, to decrease amount of venom absorbed.
Local reactions can be treated symptomatically.
Anaphylaxis is treated with epinephrine, corticosteroids, inhaled β-adrenergic agonists, and H1 and H2 antihistamines.
Patients with allergic reactions should be discharged with an EpiPen with appropriate education on its use.
Necrotizing Fasciitis
Jennifer Livingston
Carmen Rancilio
Definition
Rapidly progressing deep tissue infection involving fascial and muscle layers, skin, and subcutaneous tissue. Does not typically extend into the bone or joints.
Etiology/Types
Most commonly polymicrobial (55%-75% of cases); average of four different organisms.
Commonly associated with group A streptococci, Staph. aureus, Klebsiella species, E. coli, and other anaerobic organisms.
Varicella zoster: less common occurrence since development of varicella vaccine.
Most fulminant cases are generally associated with Streptococcus pyogenes; toxic shock syndrome and high mortality.
Pathophysiology
Destruction of skin and muscle tissue by toxins released from bacteria.
Infection progresses along the superficial fascial plane.
Clinical Presentation
May occur anywhere on the body; epidermis is often spared.
Erythema, warmth, induration, and edema of skin at local inflammatory site; rapidly progressing; fever, typically >39°C (102.2°F).
Often associated with limited mobility of nearest joint.
Marked tachycardia; hypotension in some cases; may appear toxic.
FIGURE 21.1 • Necrotizing Fasciitis Surgical Exploration. A: Surgical débridement of cervicofacial necrotizing fasciitis. A large portion of the skin of the left side of the neck was necrotic and had to be removed. Note that the skin is undermined by the infection and is dissected easily by finger pressure alone. B: An 8-year-old boy with cervicofacial necrotizing fasciitis secondary to an infected lower primary molar. Note the swelling extending from the cheek to the anterior chest wall. The chalky material on his neck is calamine lotion placed by his mother, thinking that the vesicles on the skin were poison ivy.
Presence of crepitus most commonly associated with Clostridium species or other gram-negative bacilli (rod) infections (e.g., Klebsiella, E.coli, Proteus).
May progress to gangrene and tissue sloughing as a result of tissue ischemia and necrosis.
Most common in individuals with underlying immunocompromised state (e.g., neoplasm, type 1 diabetes, recent surgical procedure).
Can occur in otherwise healthy individuals after a puncture wound, abrasion, or laceration.
Diagnostic Evaluation
CBC; leukocytosis; blood cultures: yield an organism in most cases.
Surgical exploration: involved subcutaneous tissue and fascia gray; tissue has little resistance to surgical probing (Figure 21.1).
Management
Early supportive care, fluid resuscitation, vasoactive agent support, oxygen/respiratory support.
Surgical consultation: debridement. All devitalized tissue removed. Repeat exploration often needed in 24 to 48 hours.
Intravenous antibiotic administration.
Meticulous wound care and broad-spectrum antibiotics initiated promptly.
Include aerobic (e.g., penicillin G, ampicillin-sulbactam, clindamycin) and anaerobic coverage (e.g., metronidazole, third-generation cephalosporin); consider vancomycin in communities with high rates of methicillin-resistance.
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