Rosen & Barkin's 5-Minute Emergency Medicine Consult (409 page)

May also consider:

• Infliximab
  
• Cyclosporine A
  
• Methotrexate
  

FOLLOW-UP

• Admit all patients who fulfill diagnostic criteria for Kawasaki disease
  
• Admit toxic-appearing patients who do not yet meet the criteria for Kawasaki disease
  

• Nontoxic children who do not fulfill diagnostic criteria
  
• Close follow-up is required
  

Cardiology consultation for all patients

• Prompt diagnosis and therapy can prevent coronary aneurysms in 95%
  
• Aspirin and IVIG are mainstays of therapy
  
• Must consider the diagnosis in febrile children presenting to the ED for multiple visits
  
• Restrict steroids to children with 2 IVIG failures
  

• Ashouri N, Takahashi M, Dorey F, et al. Risk factors for nonresponse to therapy in Kawasaki disease.
  J Pediatr
  . 2008;153:365–368.
  
• Gerding R. Kawasaki disease: A review.
  J Pediatr Health Care
  . 2011;25:379–387.
  
• Harnden A, Takahashi M, Burgner D. Kawasaki disease.
  BMJ
  . 2009;338:b1514.
  
• Kuo HC, Yang KD, Chang WC, et al. Kawasaki disease: An update on diagnosis and treatment.
  Pediatr Neonatol
  . 2012;53:4–11.
  
• Newburger JW, Sleeper LA, McCrindle BW, et al. Randomized trial of pulsed corticosteroid therapy for primary treatment of Kawasaki disease.
  N Engl J Med
  . 2007;356:663–675.
  
• Newburger JN,Takahashi M, GerberMA, et al. Diagnosis, treatment, and long-term management of Kawasaki disease: A statement forhealth professionals from the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young,American Heart Association.
  Pediatrics
  .2004;114:1708–1733.
  
• Scuccimarri R. Kawasaki disease.
  Pediatr Clin N Am
  . 2012;59:425–445
  
• Tacke CE, Burgner D, Kuipers IM, et al. Management of acute and refractory Kawasaki disease.
  Expert Rev Anti Infect Ther
  . 2012;10:1203–1215.
  

See Also (Topic, Algorithm, Electronic Media Element)

Myocardial Infarction

CODES

• 429.0 Myocarditis, unspecified
  
• 446.1 Acute febrile mucocutaneous lymph node syndrome [MCLS]
  
• 447.6 Arteritis, unspecified
  

BASICS

• Defined by the position of the tibia in relation to the distal femur:
  
  • Anterior dislocation:
    
    • Most common dislocation, accounts for 60%
      
    • Hyperextension of the knee
      
    • Rupture of the posterior capsule at 30°
      
    • Rupture of the posterior cruciate ligament (PCL) and popliteal artery (PA) occurs at 50°
      
  • Posterior dislocation:
    
    • Direct blow to the anterior tibia with the knee flexed at 90°, “dashboard injury”
      
    • Anterior cruciate ligament (ACL) is usually spared.
      
  • Medial dislocation:
    
    • Varus stress causing tear to the ACL, PCL, and lateral collateral ligament (LCL)
      
  • Lateral dislocation:
    
    • Valgus stress causing tear to the ACL, PCL, and medial collateral ligament (MCL)
      
• Associated injuries:
  
  • PA injury:
    
    • Occurs in 35% of dislocations.
      
    • Anterior dislocations place traction on PA and cause contusion or intimal injury, which may result in delayed thrombosis.
      
    • Posterior dislocations cause direct intimal fracture and transection of the artery with immediate thrombosis.
      
  • Peroneal nerve injury:
    
    • Less common than PA injury
      
    • If present, must rule out concomitant arterial insult
      
    • Medial dislocation causes injury by traction of the nerve.
      
    • Rotary injuries have a high incidence of traction and transection.
      

High-energy injuries such as motor vehicle crashes, auto–pedestrian accidents, and athletic injuries (football most common)

DIAGNOSIS

• Grossly deformed knee
  
• Grossly unstable knee in AP plane or on varus/valgus stress
  
• Lack of distal pulse:
  
  • PA injury is primary concern.
    
• Signs of distal ischemia:
  
  • Pallor, paresthesia, pain, paralysis
    

Mechanism of injury with high level of suspicion

• Distal pulses
  
• Distal nerve function:
  
  • Hypesthesia of 1st web space, inability to dorsiflex foot
    
• Ligamentous laxity
  

• History of mechanism of injury
  
• Complete and careful physical exam:
  
  • Pulses—palpation, Doppler, ankle–brachial index (ABI), and cap refill
    
  • Neurologic—sensation to 1st web space and great toe, movement of toes, dorsiflexion of foot
    
• AP and lateral knee radiographs
  
• Documented repeat exam if any closed reduction is attempted
  

• AP/lateral radiograph of knee:
  
  • Essential to rule out concomitant fractures
    
• MRI within 1 wk of injury to define ligamentous injury
  

• ABI—likelihood of significant arterial injury requiring surgery low if ≥0.9
  
• Peripheral vascular ultrasonography
  
• Arteriogram should be considered:
  
  • High suspicion of PA injury
    
  • Poor pulses or distal perfusion after reduction
    
  • Peroneal nerve injury
    
  • Ischemic symptoms despite normal pulses
    

• Tibial plateau fracture
  
• Supracondylar femoral fracture
  
• Ligamentous/tendonous avulsion fracture
  

TREATMENT

• Management of ABCs
  
• Documentation of pulses and motor response essential
  
• Splint knee in slight flexion to prevent PA traction or compression.
  

• ABCs especially when motor vehicle crash or auto–pedestrian accident
  
• Fluid resuscitation; hypotension may alter distal pulses and perfusion.
  
• Closed reduction immediately for any limb ischemia
  
• Early surgical consult in an open injury or high suspicion of arterial injury
  

• Closed reduction by longitudinal traction and lifting femur into normal alignment without placing pressure on popliteal fossa
  
• Posterior leg splint/knee immobilizer with knee in 15–20° of flexion
  
• Repeat neurovascular exam after manipulation and at frequent intervals.
  
• IV analgesia for patient comfort
  
• Surgical consult (orthopedic and vascular): Open injury, PA injury, or unable to reduce