Rosen & Barkin's 5-Minute Emergency Medicine Consult (54 page)

Bone marrow biopsy evaluates:

• Aplastic anemia
  
• Myelodysplasia
  
• Bone marrow malignancy
  
• Myeloproliferative disorders
  

• Acquired versus inherited anemia
  
• Anemia of chronic disease
  
• Blood loss
  
• CHF
  
• Dilutional anemia
  
• Hemolysis
  
• Malignancy
  
• Nutritional deficiency/malabsorption
  
• Toxic bone marrow suppression
  

• Hemolytic anemia of the newborn:
  
• Rh antibody crosses placenta when Rh-negative mother has Rh-positive child.
  

• Physiologic or dilutional anemia in 3rd-trimester pregnancy:
  
• 25% increase of RBC mass and 50% increase in plasma volume
  

• Values for Hgb/Hct in healthy elderly are generally lower than in younger adults.
  
• This lower “normal” must be a diagnosis of exclusion.
  

TREATMENT

Ongoing blood loss requires close assessment and rapid transport:

• Control bleeding to include wound packing and use of tourniquets if needed.
  
• Two large-bore IVs
  

• Airway, breathing, circulation (ABCs)
  
• Oxygen
  
• IV fluid resuscitation with 0.9% NS if ongoing loss/hypotension
  

• Depends on severity of anemia and acuteness of onset
  
• Transfusion for hemorrhage with unstable vital signs not responding to crystalloid resuscitation.
  
• Most anemias seen in ED are chronic and do not require immediate intervention.
  
• Therapy for specific anemia:
  
  • Iron deficiency:
    
    • FeSO
      ₄
      : 300 mg PO TID
      
    • Investigate underlying cause.
      
    • Increased Hgb expected in 2–3 wk
      
  • Renal failure:
    
    • Endogenous erythropoietin is diminished.
      
    • Replace with recombinant erythropoietin
      
  • Autoimmune hemolytic anemia:
    
    • Corticosteroids (prednisone 60 mg/day until response)
      
    • Immunosuppressive agents
      
    • Plasmapheresis
      
    • Splenectomy if splenic sequestration
      
  • Drug-induced hemolytic anemia: Stop offending agent.
    
  • Anemia of chronic disease: Treat underlying disease.
    
  • Vitamin B
    ₁₂
    deficiency:
    
    • Vitamin B
      ₁₂
      : 1,000 μg IM daily for 1 wk, then weekly for 1 mo, then monthly
      
    • Hematologic parameters normalize within 2 mo.
      
    • Neurologic symptoms present >6 mo may be permanent.
      
  • Folate deficiency:
    
    • Folic acid: 1 mg PO daily
      
  • Aplastic anemia
    
  • Antithymocyte globulin
    
  • Bone marrow transplantation:
    
    • Sickle cell anemia
      
    • Supportive care with oxygen, rehydration, analgesia
      
    • Treat precipitating cause.
      
  • Leukemia:
    
    • Bone marrow replacement
      

• Iron supplements
  
• Erythropoietin for renal failure
  
• Corticosteroids for autoimmune
  
• Vitamin B
  ₁₂
  
• Folic acid (B
  ₉
  )
  

FOLLOW-UP

• Unstable vital signs
  
• Ongoing blood loss
  
• Symptomatic anemia—angina/dyspnea/syncope/neurologic symptoms
  
• Need for transfusion
  
• Need for aggressive evaluation
  
• Severe anemia
  
  • Initial, unexplained Hgb <8 g/dL
    
  • Major difficulty in obtaining outpatient care for patients whose Hgb are significantly low or when comorbidity is present
    

Discharge vast majority of stable patients for outpatient workup.

Newly diagnosed anemic patients need to be worked up:

• If stable for discharge from the ED, provide follow-up options for workup
  

• Anemia is an indication of an underlying disorder or deficiency.
  
• Severe or life-threatening cases require immediate correction via blood transfusion.
  
• Most cases seen in the ED are chronic and do not require immediate intervention.
  

• Bryan L, Zakai N. Why is my patient anemic?
  Hematol Oncol Clin N
  . 2012;26:205–230.
  
• Bunn HF.
  Goldman: Goldman’s Cecil Medicine
  . 24th ed. Philadelphia, PA: Saunders, an imprint of Elsevier Inc.; 2011.
  
• Hoffman R, Benz EJ Jr, Silberstein LE, et al.
  Hematology: Basic Principles and Practice
  . 6th ed. Philadelphia, PA: Saunders, an imprint of Elsevier Inc.; 2012.
  
• Recht M. Thrombocytopenia and anemia in infants and children.
  Emerg Med Clin North Am
  . 2009;27:505–523.
  
• Rizack T. Special hematologic issues in the pregnant patient.
  Hematol Oncol Clin N
  . 2012;26:409–432.
  

See Also (Topic, Algorithm, Electronic Media Element)

• GI Bleeding
  
• Renal Failure
  
• Sickle Cell Disease
  

CODES

• 280.0 Iron deficiency anemia secondary to blood loss (chronic)
  
• 285.1 Acute posthemorrhagic anemia
  
• 285.9 Anemia, unspecified
  

BASICS

• Nonpruritic, well-demarcated, nonpitting edema of the dermis
  
• Due to the release of inflammatory mediators that cause dilation and increased permeability of capillaries and venules:
  
  • Mast cell mediated
    
  • Kinin related from the generation of bradykinin and complement-derived mediators
    
• Similar in pathologic basis to urticaria except that affected tissue lies deeper:
  
  • Urticaria affects superficial tissue and causes irritation to mast cells and nerves in the epidermis leading to intense itching.
    
  • Angioedema occurs in deeper layers, which have fewer mast cells and nerves, therefore causing less itching.
    
  • Angioedema can affect tissues other than the skin, for example, the gut.
    
  • Angioedema may be seen in a mixed picture along with urticaria
    
• Hereditary and acquired etiologies are due to deficiencies in the quantity and/or function of C1-INH rather than classic hypersensitivity reactions
  
• Hereditary angioedema (HAE):
  
  • An autosomal dominant disorder caused by a deficiency of C1-INH
    
  • The prevalence of HAE is estimated to range from 1:10,000 to 1:150,000.
    
  • C1-INH has a regulatory role in the contact, fibrinolytic, and coagulation pathways.
    
  • Deficiency results in unregulated activity of the vasoactive mediators bradykinin, kallikrein, and plasmin.
    
  • More than 100 mutations of the C1-INH gene have been reported.
    
  • Type 1: Decreased expression of C1-INH
    
  • Type 2: Normal plasma levels of C1-INH but the protein is dysfunctional
    
  • Type 3: Mutation in coagulation factor XII resulting in increased kinin production:
    
    • Symptoms increased by estrogen-containing medications
      
  • Episodes occur in all 3 types when inflammation, trauma, or other factors lead to depletion of C1-INH.
    
• Acquired angioedema:
  
  • Normal quantities and function of C1-INH
    
  • Type 1 is associated with lymphoproliferative diseases and caused by consumption of the C1-INH protein by malignant cells.
    
  • Type 2 is autoimmune caused by circulating antibodies that inactivate C1-INH.
    
• ACE inhibitor–induced angioedema:
  
  • Accounts for 2030% of all angioedema cases presenting to ER reported in 0.1–2.2% of patients taking ACE inhibitors
    
  • Usually occurs during the 1st mo of taking the medication, however the 1st event may occur spontaneously after many years.