Rosen & Barkin's 5-Minute Emergency Medicine Consult (651 page)

• Lumbar puncture if CNS infection or subarachnoid hemorrhage is suspected
  
• Arthrocentesis for acute arthritis
  

• Sickle cell crises may mimic or obscure more serious underlying pathology (e.g., acute abdomen, MI, PE, nephrolithiasis)
  
• Suspect other diagnoses if pain is more severe or atypical
  

TREATMENT

• Identify and treat high morbidity complications
  
• Establish venous access
  
• Assess pain and initiate therapy
  

• Choice of analgesics dependent on patient, severity of presentation, and prior agents:
  
  • Reassess pain frequently (e.g., every 15–30 min) and titrate until improvement
    
  • IV opiates (e.g., morphine, hydromorphone, fentanyl) 1st line, consider adjunct agents
    
  • Adjuncts: Acetaminophen, NSAIDs (use with caution given impaired renal function)
    
  • Caution with meperidine as metabolites may accumulate and pose seizure risk
    
  • If no venous access, PO and subcutaneous analgesics preferred over IM
    
• Hydration:
  
  • Oral hydration if patient tolerating po
    
  • Parenteral IV solution 0.45% NS for adults and children or 0.2% NS for infants
    
  • Avoid over-hydration, at risk for:
    
    • Hyperchloremic metabolic acidosis which promotes RBC sickling
      
    • Atelectasis which precipitates acute chest syndrome
      
• Complication-specific therapy:
  
  • Acute chest syndrome:
    
    • Oxygen, bronchodilators, incentive spirometer
      
    • Consider exchange transfusion for worsening respiratory symptoms, hypoxemia, and increasing A–a gradient
      
  • Splenic sequestration:
    
    • Simple transfusion, promotes remobilization of RBCs
      
    • Be aware risk of precipitating VOC after raising Hb levels
      
    • Ideal treatment is prevention: Chronic transfusions, splenectomy
      
  • Aplastic crisis:
    
    • Simple transfusion
      
    • Isolation from pregnant healthcare workers
      
  • Priapism:
    
    • 1st line: Intracavernosal aspiration with α-adrenergic agonist (e.g., epinephrine, terbutaline) irrigation
      
    • 2nd line: Exchange transfusion if failed aspiration
      
  • Empiric antibiotics: Sepsis, pneumonia, and osteomyelitis
    
  • Exchange transfusion may be required for complications such as CVA and priapism
    
• Consultations:
  
  • Hematology especially if exchange transfusion required
    
  • Neurology/neurosurgery for acute CNS events
    
  • Urology for priapism
    

FOLLOW-UP

• Refractory pain
  
• Complications: Acute chest syndrome, sequestration crisis, aplastic crisis, CVA/TIA, refractory priapism
  
• Signs of bacterial infection or fever of undetermined etiology
  
• Symptomatic anemia
  
• ICU admission for hemodynamic instability, worsening hypoxemia in acute chest syndrome, and severe acute CNS events.
  

• Resolution of pain crisis
  
• No indications for admission
  
• Follow-up arranged with hematologist
  

Meticulous primary care can limit the frequency and severity of pain crises.

If discharged, patient should see PCP or hematologist in 1–2 days.

• Distinguish typical sickle cell crisis from acute life-threatening complications
  
• Treat pain aggressively with appropriately selected and administered analgesic agents
  
• Patients with acute pain may not demonstrate typical signs, such as tachycardia or diaphoresis
  

• Glassberg J. Evidence-based management of sickle cell disease in the emergency department.
  Emerg Med Pract.
  2011;13(8):1–20.
  
• Montelambert MD. Management of sickle cell disease.
  BMJ.
  2008;337:626–630.
  
• Rees DC, Williams TN, Gladwin MT. Sickle-cell disease.
  Lancet.
  2010;376:2018–2031.
  
• Rogers DT, Molokie R. Sickle cell disease in pregnancy.
  Obstet Gynecol Clin North Am.
  2010;37:223–237.
  
• Wang W, et al. Sickle cell anemia and other sickling syndromes. In: Greer J, ed.
  Wintrobe’s Clinical Hematology.
  12th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2009:1038–1082.
  
• http://scinfo.org
  .
  
• http://www.cdc.gov/NCBDDD/sicklecell/index.html
  .
  

See Also (Topic, Algorithm, Electronic Media Element)

Anemia

CODES

• 282.41 Sickle-cell thalassemia without crisis
  
• 282.61 Hb-SS disease without crisis
  
• 282.63 Sickle-cell/Hb-C disease without crisis
  

BASICS

• Inflammation of mucous membranes lining the paranasal sinuses and nasal passages with or without fluid collection in the sinus cavities
  
• Classifications:
  
  • Acute: Signs and symptoms for <4 wk
    
  • Subacute: Signs and symptoms for 4–8 wk
    
  • Chronic: Signs and symptoms for >8 wk in spite of antibiotic treatment
    
  • Recurrent: 3 or more episodes per year
    

• Acute rhinosinusitis pathophysiology:
  
  • Viral upper respiratory infection or allergies causes mucous membrane inflammation
    
  • Inflammation causes obstruction of sinus ostia, decreased mucociliary clearance, and thickening of secretions
    
  • Viruses are the primary cause, but 0.5–2.2% develop into bacterial infection after bacteria become trapped and multiply, resulting in suppuration
    
  • Nosocomial rhinosinusitis associated with nasogastric and nasotracheal tubes
    
  • Immunocompromised patients at higher risk for rhinosinusitis
    
• Subacute and chronic rhinosinusitis pathophysiology:
  
  • Multifactorial, role of bacteria remains elusive
    
  • Allergic inflammation causing narrowed ostia and blocked drainage
    
  • Immune dysfunction leading to increased infectious risk
    
  • Impaired ciliary function leading to decreased mucous clearance
    
  • Odontogenic infection causing maxillary sinusitis
    
  • Fungus ball
    
  • Anatomical obstruction or polyps obstructing sinus ostia
    
• Microbiology:
  
  • Acute rhinosinusitis:
    
    • Nontypable
      Haemophilus influenzae
      
    • Streptococcus pneumoniae
      
    • Moraxella catarrhalis
      
    • Staphylococcus aureus
      
    • Anaerobes
      
    • Viruses: Parainfluenza, adenovirus, rhinovirus, influenza
      
  • Chronic rhinosinusitis:
    
    • Same as acute, often polymicrobial, with increasing anaerobes and gram negatives
      
  • Nosocomial rhinosinusitis:
    
    • S. aureus
      
    • Streptococcal species
      
    • Pseudomonas
      
    • Klebsiella
      
  • Immunocompromised patients with rhinosinusitis:
    
    • Bacteria as above
      
    • Fungal pathogens (
      Aspergillus
      )
      

• Nontypable
  H. influenzae
  more common than
  S. pneumoniae
  as cause of acute bacterial rhinosinusitis in children
  
• Ethmoid and maxillary sinuses present at birth
  
• Frontal and sphenoid sinuses do not emerge until age 6–7 yr
  
• Rhinosinusitis more common in children
  
• Periorbital/orbital cellulitis is a common complication of ethmoid rhinosinusitis in children:
  
  • Periorbital swelling, fever, ptosis, proptosis, and painful or decreased extraocular movements