Rosen & Barkin's 5-Minute Emergency Medicine Consult (727 page)

• ECG – evaluate for thrombogenic rhythms such as atrial fibrillation
  
• Echocardiography in patients with no other cause for TIA – exclude existing thrombus and abnormal wall motion or aneurysms that cause thrombus
  

• Hypoglycemia
  
• Seizure
  
• Paralysis after seizure (Todd's paralysis)
  
• Atypical migraine
  
• Psychiatric disease
  
• Stroke
  
• CNS tumors or metastases
  
• Subdural hemorrhage
  
• Subarachnoid hemorrhage
  
• Multiple sclerosis
  
• Intracerebral hemorrhage
  
• Air embolism
  
• Vasculitis
  
• Arterial dissection
  

• Congenital heart disease
  
• Vasculitis
  
• Arterial dissection
  
• Sickle cell disease
  
• Neurocutaneous syndromes
  
• Vascular malformations
  
• Meningitis
  

TREATMENT

• Rapid assessment of neurologic deficits
  
• Consider transport to a stroke center, when available, if deficits persist
  

• IV access
  
• Cardiac monitoring
  
• Supplemental oxygen if hypoxic
  

• Main goals in the management of TIA:
  
  • Improve perfusion to ischemic tissue
    
  • Prevent a subsequent stroke
    
• BP management:
  
  • BP should not be lowered acutely unless over 220/120 mm Hg
    
  • Hypertensive patients with TIA should have their BP lowered if stable at 24 hr after TIA
    
  • Key in patients upon discharge
    
  • 1st line – HCTZ or ACE inhibitor
    
• Antiplatelet therapy:
  
  • All patients, in the absence of contraindications, need antiplatelet therapy for stroke prevention
    
  • 1st line – aspirin (ASA):
    
    • Safe, cheap, effective
      
  • ASA allergy – clopidogrel, ticlopidine
    
  • ASA/dipyridamole may be more effective than ASA alone
    
• Anticoagulation:
  
  • Indicated for new onset atrial fibrillation or existing atrial fibrillation not on anticoagulants
    
  • Options include heparin/low-molecular-weight heparin with a transition to warfarin or dabigatran
    
  • The decision to anticoagulate is not emergent; discuss with admitting physician
    
• Carotid endarterectomy (CEA):
  
  • CEA within 2 wk after TIA in patients with >70% carotid stenosis reduces stroke risk by 10–15%
    
• Lipid therapy:
  
  • AHA guidelines recommend statin therapy for patients with TIA with a goal LDL of under 70 mg/dL
    
  • Key in patients upon discharge
    

• Antiplatelet agents:
  
  • Aspirin 160–325 mg daily
    
  • Aspirin/dipyridamole 25 mg/200 mg daily
    
  • Clopidogrel 300 mg initially then 75 mg daily
    
• Anticoagulation:
  
  • Heparin 5,000–7,500 U IV bolus, followed by 1,000 U/h infusion OR 80 U/kg IV bolus then 18 U/kg/h
    
  • Warfarin dose is dependent on age and weight, but goal INR for atrial fibrillation is 2–3
    
  • Dabigatran 150 mg daily (normal renal function)
    
• Acute BP management:
  
  • Labetalol 20 mg IV bolus, followed by 20–80 mg IV every 10 min; max. cumulative dose of 300 mg
    
  • Nicardipine 5 mg/h infection, increase by 2.5 mg/h every 5–15 min; max. dose of 15 mg/h
    

FOLLOW-UP

• There are no clear indications for admission or discharge
  
• Patients with TIA have variable short-term risk of stroke
  
• Goal of admission is to prevent subsequent stroke in high-risk patients
  
• Scoring systems have been developed to predict short-term risk of stroke and therefore can guide disposition
  
• Most common = ABCD2 score:
  
  • Age >60 = 1 point
    
  • BP >140/90 = 1 point
    
  • Clinical features:
    
    • Unilateral weakness = 2 points
      
    • Speech difficulty alone = 1 point
      
  • Duration:
    
    • >60 min = 2 points
      
    • 10–59 min = 1 point
      
    • <10 min = 0 points
      
  • Diabetes = 1 point
    
• ABCD2 score 0–3 = low risk of stroke (∼1% at 7 days)
  
• ABCD2 score 4–5 = moderate risk for stroke (∼6% at 7 days)
  
• ABCD2 score 6–7 = high risk for stroke (∼12% at 7 days)
  
• Patients with moderate to high risk for short-term stroke = admission
  
• Patients with low risk for short-term stroke, but poor follow-up = observation unit
  

All children with TIA should be admitted for close neurologic observation, with strong consideration of ICU level care

• No clear discharge criteria exist:
  
  • Low risk for short-term stroke, with good follow-up
    

• The risk of stroke after TIA is highest within 2 days of symptoms
  
• Discharged patients need to see neurology/primary care within 24–48 hr
  

• Primary Care/Neurology – management of risk factors for cerebrovascular disease (hypertension, diabetes, etc.)
  
• Vascular surgery – for carotid stenosis. Follow-up within 1 wk, plan for possible CEA within 2 wk
  
• Cardiology – for those patients with cardiac cause of stroke, such as atrial fibrillation or cardiomyopathy
  

• Pearls:
  
  • Risk stratification scores (such as ABCD2) can help guide disposition
    
  • Patients with carotid stenosis need rapid vascular surgery follow-up
    
• Pitfalls:
  
  • Failure to recognize the subtle lacunar TIA syndromes, such as sensory loss
    
  • Failure to rapidly check a glucose in a patient with a focal neurologic deficit
    
  • Discharging patients with TIA without close outpatient follow-up
    

• Davis SM, Donnan GA. Clinical practice. Secondary prevention after ischemic stroke or transient ischemic attack.
  New Engl J Med
  . 2012;366:1914–1922.
  
• Panagos PD. Transient ischemic attack (TIA): The initial diagnostic and therapeutic dilemma.
  Am J Emerg Med
  . 2012;30:794–799.
  
• Pare JR, Kahn JH. Basic neuroanatomy and stroke syndromes.
  Emerg Med Clin North Am
  . 2012;30:601–615.
  
• Siket MS, Edlow JA. Transient ischemic attack: Reviewing the evolution of the definition, diagnosis, risk stratification, and management for the emergency physician.
  Emerg Med Clin North Am
  . 2012;30:745–770.
  
• Sorensen AG, Ay H. Transient ischemic attack: Definition, diagnosis, and risk stratification.
  Neuroimaging Clin N Am
  . 2011;21:303–313.
  

CODES

• 435.3 Vertebrobasilar artery syndrome
  
• 435.8 Other specified transient cerebral ischemias
  
• 435.9 Unspecified transient cerebral ischemia
  

BASICS

Immune response to a graft’s genetically dissimilar antigens resulting in rejection of the transplanted organ:

• HLA incompatibility:
  
  • Most common cause of rejection
    
  • Rejection of solid organ transplants
    
• Blood group incompatibility:
  
  • Much less of a risk to graft survival than HLA incompatibility
    
  • May result in hyperacute rejection of primarily vascularized grafts (kidney and heart)
    
• 3 phases of rejection:
  
  • Hyperacute:
    
    • Immediate postoperative period
      
    • Antibody reaction to red cells or HLA antigens
      
    • Endothelial damage
      
    • Platelets accumulate, thrombi develop, and tissue necrosis occurs.
      
    • Rare with careful donor–recipient matching
      
• Acute:
  
  • Within the 1st 3 mo postop
    
  • At any time if immunosuppressant (IS) medication is stopped
    
  • T-cell–dependent process. Inflammatory cells infiltrate allograft, release cellular and humoral factors, destroys graft
    
  • Presents with constitutional symptoms and signs of transplant organ insufficiency
    
• Chronic:
  
  • Occurs over years
    
  • Results in gradual organ failure