Rosen & Barkin's 5-Minute Emergency Medicine Consult (302 page)

• Pain
  
• Localized ecchymosis and swelling
  
• Scleral or corneal laceration
  
• Extrusion of intraocular contents
  
• Markedly decreased visual acuity
  
• Limited extraocular motion
  
• Hyphema
  
• Severe subconjunctival hemorrhage and edema, especially if circumferential bloody chemosis
  
• Abnormally deep or shallow anterior chamber
  
• Low intraocular pressure:
  
  • Note: Do not perform tonometry if there is suspected rupture.
    
• Irregular pupil (points toward lesion)
  
• Subluxed lens
  
• Commotio retinae—gray-white discoloration of the retina
  

• Mechanism of injury:
  
  • Assess for possibility of retained intraocular foreign body
    
• History of previous eye surgery
  
• Preinjury visual acuity
  
• Assess tetanus status
  
• Ascertain time of last PO intake
  

• Penlight or slit-lamp exam observing for signs of globe rupture
  
• If the diagnosis of ruptured globe is made, defer further ocular exam until the time of surgical repair:
  
  • Prevents placing any undue pressure on the eye and risking extrusion of the intraocular contents
    
• If no evidence of globe rupture on initial survey, proceed with thorough ophthalmologic exam:
  
  • Visual acuity
    
  • Slit-lamp exam
    
  • Cornea
    
  • Anterior chamber
    
  • Iris
    
  • Sclera
    
  • Fundus
    
  • Retina
    
• Seidel test: Observe if fluorescein moves away as contents (which appear yellow-green) leak out at site of rupture:
  
• Measure intraocular pressure
  
  • Perform only if globe rupture is definitely
    not
    present.
    
• Ultrasound (only if rupture not suspected)
  

Perform thorough ocular exam as outlined above:

• Once diagnosis of globe rupture is suspected or made, defer further exam until time of repair.
  

Preoperative labs:

• CBC
  
• Electrolytes
  
• Coagulation studies
  

• Orbital radiograph (anteroposterior/lateral) for metallic intraocular foreign body
  
• CT scan of the orbits (axial and coronal views)
  
• MRI scan of the orbits after retained metallic foreign body is ruled out
  
• B-scan US of the eye
  

• Slit-lamp
  
• Fluorescein
  

• Intraocular foreign body
  
• Hyphema
  
• Severe subconjunctival hemorrhage and chemosis
  
• Partial corneal laceration
  
• Partial scleral laceration
  

TREATMENT

• Place a shield (not patch) over eye with no pressure on the globe.
  
• Use a Styrofoam cup if no shield available.
  

• Keep manipulation of the eye to a minimum if ruptured globe is suspected.
  
• Try to prevent any activity that will cause an increase in intraocular pressure such as straining, coughing, or vomiting.
  

• Prepare for definitive surgical management:
  
  • Emergent ophthalmologic consultation
    
  • Thorough physical exam to identify concurrent injuries
    
  • Preoperative labs and ECG as indicated
    
  • No food or drink (NPO)
    
• Minimize intraocular pressure to reduce further injury
  
  • Administer antiemetic for nausea/vomiting
    
  • Elevate the head of the bed
    
  • Protective eye shield (NO pressure on the globe itself)
    
• Update tetanus status.
  
• Administer prophylactic antibiotics IV:
  
  • Skin organisms (staph, strep) most common
    
  • Consider injury-specific contaminants in cases of animal bites, organic foreign body, etc.
    
  • Vancomycin + ceftazidime OR vancomycin + ciprofloxacin if allergic to penicillin
    
• Succinylcholine is relatively contraindicated:
  
  • However, with a defasciculating dose of a nondepolarizing agent and sufficient anesthesia, it may be used.
    

• Consider nonaccidental trauma
  
• Because of risk of extrusion of intraocular contents, straining/crying should be avoided. Try to keep them happy!
  

• Ceftazidime: 1–2 g (peds: 30–50 mg/kg) IV q8h
  
• Ciprofloxacin: 400 mg (peds: 10 mg/kg) IV q12h
  
• Clindamycin: 450 mg (peds: 8–12 mg/kg) IV q8h
  
• Ondansetron (Zofran): 4 mg IV
  
• Prochlorperazine (Compazine): 5–10 mg IV/IM
  
• Tobramycin: 2 mg/kg (peds: 2 mg/kg) IV q8h
  
• Vancomycin: 15 mg/kg IV q8–12h (peds: 10 mg/kg IV q6h)
  

FOLLOW-UP

• All patients with globe rupture/penetrating eye injuries
  
• Early enucleation for severe injury
  

Globe penetration excluded

• Emergent ophthalmologic consultation in the ED may be needed to definitively rule out globe rupture owing to difficulty with exam and the desire to minimize manipulation of the eye.
  
• Speed is of the essence since the risk of infection increases with prolonged time to operative repair.
  
• If appropriate, patient should be counseled on use of protective eyewear to prevent recurrence.
  

Postoperative ophthalmology follow-up

• Do not manipulate the eye if you suspect or confirm a ruptured globe:
  
  • Place eye shield over affected eye.
    
• Administer antiemetic for patients with nausea and vomiting to prevent elevation of intraocular pressure and extrusion of globe contents.
  
• Update tetanus
  
• Empiric antibiotics tailored to clinical scenario
  

• Linden JA, Renner GS. Trauma to the globe.
  Emerg Med Clin North Am
  .1995;13(3):581–605.
  
• Marx JA, Hockberger RS, Walls RM, et al.
  Rosen’s Emergency Medicine
  . 7th ed. Philadelphia, PA: Saunders; 2009;863–864.
  
• Navon SE. Management of the ruptured globe.
  Int Ophthalmol Clin
  . 1995;35:71–91.
  
• Sabaci G, Bayer A,Mutlu FM, et al. Endophthalmitis after deadly-weapon-related open-globe injuries: Risk factors, value ofprophylactic antibiotics, and visual outcomes.
  Am J Ophthalmol
  .2002;133:62–69.
  
• Skarbek-Borowska SE, Campbell KT. Globe rupture and nonaccidental trauma: Two case reports.
  Pediatr Emerg Care
  . 2011;27(6):544–546.
  

See Also (Topic, Algorithm, Electronic Media Element)

• Blowout Fracture
  
• Corneal Abrasion
  
• Corneal Foreign Body
  
• Hyphema
  
• Retinal Detachment
  
• Visual Loss
  

CODES

• 871.0 Ocular laceration without prolapse of intraocular tissue
  
• 871.2 Rupture of eye with partial loss of intraocular tissue
  

BASICS

• Syndrome characterized by:
  
  • Hematuria
    
  • Proteinuria
    
  • Red blood cell casts
    
  • Hypertension
    
  • Renal insufficiency
    
• Common pathway of multiple diseases resulting in intraglomerular inflammation and cellular proliferation
  
• Contributing factors:
  
  • Genetics
    
  • Infectious
    
  • Rheumatologic
    
  • Leading to antibody deposition:
    
    • Antibody attaches to glomerular antigen (native or implanted).
      
    • Circulating antigen–antibody complex deposited
      
  • Causing an influx and activation of inflammatory mediators:
    
    • Leukocytes, complement, cytokines
      
    • Cell-mediated immune mechanisms
      
• Results in glomerular dysfunction
  
• Persistent inflammation that can lead to scarring and permanent damage.