Rosen & Barkin's 5-Minute Emergency Medicine Consult (725 page)

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See Also (Topic, Algorithm, Electronic Media Element)

• Allergic Reaction
  
• Anaphylaxis
  
• Disseminated Intravascular Coagulation
  
• Sepsis
  

CODES

• 780.66 Febrile nonhemolytic transfusion reaction
  
• 999.80 Transfusion reaction, unspecified
  
• 999.84 Acute hemolytic transfusion reaction, incompatibility unspecified
  

BASICS

• Transient global amnesia (TGA) has the following features:
  
  • Episode of amnesia with abrupt onset
    
  • No focal neurologic signs or symptoms
    
  • Temporary, severe, anterograde amnesia:
    
    • Acute inability to form new memories
      
    • Permanent memory gap after the episode
      
  • Temporary short-range retrograde amnesia:
    
    • More recent memories at more risk
      
    • Previously encoded memories unavailable only temporarily
      
  • Gradually improves until only remaining memory deficit is the gap induced by the anterograde amnesia
    
• Incidence between 3 and 8 per 100,000 people:
  
  • 75% occur in people of 50–70 yr old
    
  • TGA rare <40 yr
    
• Most attacks last between 1 and 8 hr (range 15 min–7 days)
  

• Multimodal MRI, SPECT, and PET have shown some abnormalities of regional blood flow in selectively vulnerable hippocampal structures
  
• The exact etiology of TGA is unknown; speculation is controversial
  
• Speculated causes:
  
  • Vasoconstriction due to hyperventilation:
    
    • Psychogenic hyperventilation in setting of age-related cerebrovascular autoregulatory dysfunction
      
  • Hippocampal venous congestion with Valsalva:
    
    • Ultrasonography has suggested internal jugular vein incompetence
      
  • Migraine (in younger patients)
    
• No correlation between TGA and thromboembolic cerebrovascular disease has been found
  

DIAGNOSIS

Diagnostic criteria:

• Attack must be witnessed
  
• Acute onset of anterograde amnesia
  
• No alteration in consciousness
  
• No cognitive impairment except amnesia
  
• No loss of personal information (e.g., name, birth date, address, etc.)
  
• No focal neurologic symptoms
  
• No epileptic features
  
• No recent history of head trauma or seizures
  
• Attack must resolve within 24 hr
  
• Other causes of amnesia excluded
  

• Often precipitated by stressful condition:
  
  • Cough, Valsalva
    
  • Physical exertion
    
  • Sexual intercourse
    
  • Extreme fright or shock
    
  • Intense heat or cold
    
• Patient will likely feel something is wrong:
  
  • May ask “how did I get here?”
    
  • May be repetitive in questions
    
  • Will be generally aware of attack
    
• May have other subtle transient symptoms at onset, such as headache, dizziness, nausea
  
• Historical features helpful in excluding other diagnoses are:
  
  • Onset of attack witnessed, with no seizure activity or epileptiform features noted
    
  • No history of seizures in prior 2 mo
    
  • No history of recent traumatic brain injury
    
  • Acute anterograde amnesia with relatively preserved remote memory
    

• Marked anterograde amnesia
  
• Most cases (≥90% in case series) will demonstrate repetitive questioning
  
• Neurologic and general exam normal
  
• TGA patient
  WILL NOT
  be:
  
  • Somnolent
    
  • Inattentive
    
  • Globally confused
    
  • Confabulate
    
• TGA patient
  WILL
  be:
  
  • Oriented to name, birth date, address, phone number, date
    
  • Able to perform complex tasks and following complex commands
    
• Aphasia, apraxia, and agnosia are NOT findings consistent with TGA
  

• True TGA can be diagnosed with a careful history and physical exam alone
  
• If clinical diagnosis is certain, no other workup is essential
  

Testing indicated only when the diagnosis is uncertain

• CBC, comprehensive chemistries including glucose, LFTs, NH
  ₃
  , thyroid studies, and UA for organic–metabolic etiologies were implicated
  
• Tox screen, alcohol level for toxic etiologies were suspected
  

• Consider MRI if indicated.
  
  • In true TGA, MRI may show a focal hippocampal DWI or T2 lesion that resolves over time
    
• Head CT for intracranial mass if indicated
  

• EEG for seizure or nonconvulsive status if suspected
  
• Lumbar puncture and CSF analysis for encephalitis if suspected
  

• Other entities may present somewhat similarly but will likely have historical or physical exam features that readily distinguish them from TGA:
  
  • Anterior choroidal artery or posterior cerebral artery or TIA:
    
    • Additional related neurologic signs such as hemianopia
      
  • Acute confusional state/Korsakoff syndrome/metabolic disorder:
    
    • Alcohol, medication, or toxin ingestion
      
    • Decreased attention or other findings of an encephalopathy
      
    • Impairment with serial 7s or spelling “world” backward
      
    • Able to lay down new memory if allowed time to encode
      
  • Complex partial seizures/epileptic amnestic attacks:
    
    • Witnessed epileptiform activity or features (e.g., blank stares, automatisms, lip-smacking, olfactory hallucinations)
      
    • Short duration (typically <30 min; TGA lasts hours)
      
    • No repetitive questioning
      
    • Frequent and rapid recurrences
      
  • Psychogenic amnesia:
    
    • Younger patient with a known psychiatric stressor
      
    • Prominent retrograde amnesia
      
    • Psychogenic memory loss for personal identification, name, birth date, etc.
      
  • Temporal lobe brain lesion or encephalitis affecting the temporal lobe:
    
    • Has other associated neurologic symptoms (e.g., visual field cut, confusion)
      
    • Progressive and permanent amnesia
      
  • Previously unrecognized Alzheimer dementia:
    
    • Memory loss for personal information such as date, phone number, address
      
    • Signs of additional global cognitive impairment
      

TREATMENT

There are no considerations in true TGA that are specific to the pre-hospital environment