Rosen & Barkin's 5-Minute Emergency Medicine Consult (662 page)

TREATMENT

• Loosely immobilize wound site
  
• Elevate the affected extremity
  
• Cover bite with cool compresses
  
• Transport to hospital when patient experiences immediate onset of symptoms
  
• Supportive measures for patients with systemic symptoms
  

IV fluids, oxygen, cardiac monitoring if the patient is experiencing signs of systemic collapse

• Cleanse the bite site thoroughly
  
• Tetanus prophylaxis
  
• Analgesics
  
• Antibiotics:
  
  • Appropriate if wound appears infected
    
  • Not indicated prophylactically
    
  • Antistaphylococcal
    
• Dapsone:
  
  • Controversial: Consider for severe toxicity.
    
  • Screen for G6PD deficiency before initiating
    
  • Monitor for methemoglobinemia, hemolysis, and leukopenia during therapy
    
• Excision of necrotic wound:
  
  • Not indicated in the 1st 8 wk because may cause more severe ulcer formation
    
• Hemoglobinuria:
  
  • Treated with IV fluids and alkalinization
    
  • Monitor renal, fluid, and electrolyte status
    
• Dialysis for renal failure
  
• Pressors for shock state
  
• Blood products in severe hemolysis, DIC
  
• Specific antivenin:
  
  • Not commercially available
    
  • Not FDA approved for use in US
    
• Therapies requiring further investigation:
  
  • Topical or systemic steroids
    
  • Hyperbaric therapy (has been shown to decrease wound size in animal model)
    
  • Topical nitroglycerin
    
  • Negative pressure wound therapy, or vacuum-assisted closure
    

• Antibiotics:
  
  • Clindamycin: 150–300 mg PO q6h (peds: 8–16 mg/kg/d PO div. QID)
    
  • Severe skin infections:
    
    • Vancomycin: 1 g IVPB q12h (peds: 10 mg/kg q6h)
      
• Dapsone: Progressive dosage of 50–200 mg/d (peds: 2 mg/kg/24 h PO)
  
• Methylprednisolone: 125 mg IV bolus followed by prednisone 30–50 mg/d for 5 days (peds: methylprednisolone 1–2 mg/kg IV, prednisone 1–2 mg/kg PO)
  
• Morphine sulfate: 2–10 mg (peds: 0.1 mg/kg) IV or IM PRN
  

• Use dapsone only in severe cases because of increased potential for side effects such as:
  
  • Hepatitis
    
  • Methemoglobinemia
    
  • Hemolytic anemia
    
  • Leukopenia
    

FOLLOW-UP

• Significant local reaction or signs of systemic toxicity
  
• Lower threshold for children, patients with significant comorbidities
  

• No evidence of systemic toxicity or severe progression of local wound necrosis after envenomation
  
• Daily reassessment by primary physician, including blood work, until 3–4 days after envenomation to evaluate for systemic toxicity
  
• Patients should be advised about prolonged course for skin healing with consideration for surgical excision after 8 wk
  
• Patients should be advised about potential for extensive scarring, infection, and recurrent ulceration
  

Longer observation period or admission because of the higher mortality in this population

Consider consultation with:

• General surgery or plastic surgery for wound management
  
• Hyperbaric specialist for wound management
  
• Toxicologist
  
• Nephrologist for cases of renal failure
  
• Intensivist in cases of shock or DIC
  

• Primary care physician for continued evaluation of wound
  
• General surgery or plastic surgery for management of complicated wounds
  
• Hyperbaric specialist for wound management
  

• Remember the limited range of brown recluse spiders and the rarity of arachnidism as a cause of necrotic skin wounds
  
• In the absence of a reliable spider bite by history, other diagnoses must be carefully sought and excluded
  
• Be sure to screen for G6PD deficiency as it causes methemoglobinemia and hemolysis in patients receiving dapsone
  
• Have a low threshold for admitting pediatric patients, adults with systemic symptoms, or anyone with a large, painful, or infected wound
  

• Furbee RB, Kao LW, Ibrahim D. Brown recluse spider envenomation.
  Clin Lab Med
  . 2006;26(1):211–226.
  
• Mold JW, Thompson DM. Management of brown recluse spider bites in primary care.
  J Am Board Fam Pract
  . 2004;17:347–352.
  
• Swanson DL, Vetter RS. Bites of brown recluse spiders and suspected necrotic arachnidism.
  N Eng J Med
  . 2005;352:700–707.
  
• Wong SC, Defranzo AJ, Morykwas MJ, et al. Loxoscelism and negative pressure wound therapy (vacuum-assisted closure): A clinical case series.
  Am Surg
  . 2009;75(11):1128–1131.
  

See Also (Topic, Algorithm, Electronic Media Element)

Spider Bite, Black Widow

CODES

989.5 Toxic effect of venom

BASICS

• Anterior cord syndrome:
  
  • Results from flexion or axial loading mechanism or direct cord compression from vertebral fractures, dislocations, disc herniation, tumor, or abscess
    
  • Rarely, can be caused by laceration or thrombosis to the anterior spinal artery
    
• Brown-Séquard syndrome:
  
  • Hemisection of the spinal cord, classically as a result of a penetrating wound
    
  • Rarely unilateral cord compression
    
• Central cord syndrome:
  
  • Most commonly occurs in elderly patients who have pre-existing cervical spondylosis and stenosis
    
  • Forced hyperextension causes buckling of the ligamentum flavum, creating a shearing injury to the central portion of the spinal cord.
    
• Dorsal cord syndrome:
  
  • Associated with hyperextension injuries
    
• Complete cord syndrome:
  
  • Blunt or penetrating trauma that results in complete disruption of spinal cord
    
  • Symptoms that remain >24 hr generally are permanent.
    

• Spinal cord syndromes result from localized disruption of neurotransmission and exhibit mixed motor and sensory deficits. The most common mechanism is trauma.
  
• Patients with arthritis, osteoporosis, metastatic disease, or other chronic spinal disorders are at risk of developing spinal injuries as the result of minor trauma.
  

DIAGNOSIS

Acute loss of motor and/or sensory function usually following a traumatic event

• Anterior cord syndrome:
  
  • Bilateral spastic paralysis and loss of pain and temperature sensation below the level of the lesion
    
  • Preservation of dorsal column function (proprioception and position sense)
    
• Brown-Séquard syndrome (lateral cord syndrome):
  
  • Ipsilateral spastic paresis and loss of dorsal column function (proprioception and position sense)
    
  • Contralateral loss of pain and temperature sensation
    
  • Deficits usually begin 2 levels below the injury.
    
• Central cord syndrome:
  
  • Loss of motor function affects upper extremities more severely than lower extremities.
    
  • Most profound deficits occur in the distal upper extremities.
    
  • Sensory loss is more variable.
    
• Dorsal cord syndrome:
  
  • Loss of proprioception, position sensation, and coordination below the level of the lesion
    
• Complete cord syndrome:
  
  • Flaccid paresis below the level of the injury
    
  • Low BP and heart rate, flushed skin, priapism may be present (loss of sympathetic tone).
    
• Sensory deficit levels:
  
  • C2: Occiput
    
  • C4: Clavicular region
    
  • C6: Thumb
    
  • C8: Little finger
    
  • T4: Nipple line
    
  • T10: Umbilicus
    
  • L1: Inguinal region
    
  • L5: Dorsum of the foot
    
  • S5: Perianal area
    
• Motor deficit levels:
  
  • C5: Elbow flexion
    
  • C7: Elbow extension
    
  • C8: Finger flexion
    
  • T1: Finger abduction
    
  • L2: Hip flexion
    
  • L3: Knee extension
    
  • L4: Ankle dorsiflexion
    
  • S1: Ankle plantar flexion