Anemia in the Critical Care Patient
Thomas G. DeLoughery
I. EPIDEMIOLOGY OF ANEMIA IN CRITICALLY ILL PATIENTS
A. Ninety-five percent of patients admitted to intensive care settings become anemic.
B. Half of the patients in the intensive care unit (ICU) will receive red cell transfusion.
C. Most common etiologies.
1. Inflammation (i.e., anemia of chronic disease).
2. Blood loss.
3. Hemolysis.
II. CLASSIFICATION OF ANEMIA
A. Indices—classifies anemia by size of red cells (measured in femtoliters, fL).
1. Microcytic (<80 fL)—caused by interfering with hemoglobin production.
a. Iron deficiency.
b. Anemia of chronic disease.
i. Thirty percent of cases are microcytic.
ii. Etiology: inhibition of iron delivery to developing red cells.
c. Thalassemia.
d. Sideroblastic anemia.
2. Macrocytic anemia.
a. Two forms:
i. Round macrocytes—excess red blood cell (RBC) membrane.
(a) Liver disease.
(b) Alcohol abuse.
(c) Renal disease.
ii. Oval macrocytes due to interference with DNA synthesis.
(a) Megaloblastic anemia (e.g., B12 and folate deficiency).
(b) Myelodysplastic syndrome.
(c) Chemotherapeutic agents.
B. Mechanism.
1. Blood loss.
2. Hemolysis.
3. Production defects.
a. Nutritional deficiencies.
b. Anemia of chronic disease.
c. Erythropoietin deficiency (e.g., in renal insufficiency).
d. Aplastic anemia/pure red cell aplasia.
e. Myelodysplastic syndromes.
f. Thalassemias.
III. ANEMIA DUE TO BLOOD LOSS
A. Overt blood loss (e.g., trauma, gastrointestinal bleeding).
B. Subtle blood loss (e.g., through routine phlebotomy for laboratory testing).
1. Average ICU daily blood loss may approximate up to 240 mL/day in some patients.
2. Minimize laboratory draws and “batch” laboratory testing.
IV. HEMOLYTIC ANEMIA: BASIC PRINCIPLES
A. Many processes lead to destruction of red cells (see individual disorders, in subsequent text).
B. Laboratory diagnosis—can be difficult to assess hemolysis if it is subtle or patient has other abnormalities.
1. Indirect bilirubin—sensitive but not specific.
a. Elevated in liver disease and Gilbert syndrome.
2. Lactate dehydrogenase (LDH)—sensitive but not specific.
a. Elevated in liver disease, myocardial infarctions, and rhabdomyolysis.
3. Haptoglobin—specific but not sensitive.
a. Acute-phase reactant.
b. In 2% of the population haptoglobin is genetically absent.
4. Coombs test (i.e., direct antiglobulin test)—sensitive but not specific for autoimmune hemolytic anemia.
a. False positives are seen in renal disease, human immunodeficiency virus (HIV), and liver disease, and in patients who have received intravenous (IV) immunoglobulin.
V. ACQUIRED HEMOLYTIC ANEMIAS
A. Autoimmune.
1. Warm antibody.
a. Clinical presentation: acute onset of severe anemia; patient can complain of back pain and dark urine.
b. Risk factors: lupus, chronic lymphocytic leukemia, or idiopathic
c. Diagnostic testing.
i. Coombs test: immunoglobulin G (IgG) positive ± C3d positive.
d. Therapy.
i. Corticosteroids—prednisone 1 mg/kg daily.
ii. Transfusions: can be difficult to cross-match; choose “least incompatible” units.
iii. Refractory cases—rituximab or splenectomy.
2. Cold agglutinin disease.
a. Clinical presentation: anemia of variable severity, often worse in cold weather; acrocyanosis often present.
b. Risk factors.
i. Acute—sequelae of viral illness (e.g., mycoplasma).
ii. Chronic—lymphoproliferative disease.
c. Diagnostic testing.
i. Coombs test: C3d positive, IgG negative.
d. Therapy.
i. Corticosteroids, splenectomy typically ineffective.
ii. Rituximab may be effective.
iii. Plasma exchange for cases of severe anemia.
iv. Avoidance of cold if anemia mild or moderate and compensated.
v. If transfusion required need to warm blood.
3. Drug induced.
a. Clinical presentation: acute onset of anemia in the setting of exposure to one or more offending drugs.
b. Risk factors: exposure to offending drugs (Table 92-1).
c. Diagnostic testing.
i. Coombs test: positive (usually IgG).
d. Therapy.
i. Stop offending agent.
ii. RBC transfusions.
iii. Immunosuppression with corticosteroids rarely is required.
B. Microangiopathic (also see Thrombocytopenia, Chapter 89).
1. Clinical presentation—hemolytic anemia of variable severity accompanied by schistocytosis on blood smear, and markedly elevated LDH.
2. Thrombotic thrombocytopenic purpura.
a. Clinical features: microangiopathic anemia, thrombocytopenia, end-organ damage (e.g., renal, central nervous system [CNS], cardiac).
b. Risk factors: HIV, lupus, congenital.
c. Diagnostic testing.
i. Blood smear with corroborative clinical features.
ii. Very low levels of ADAMTS13 specific, but often not immediately available.
d. Therapy: plasma exchange ± corticosteroids.
3. Hemolytic uremic syndrome.
a. Clinical features: microangiopathic anemia, thrombocytopenia, renal failure.
b. Risk factors: preceding enterohemorrhage Escherichia coli gastroenteritis.
c. Diagnostic testing.
i. Blood smear with corroborative clinical features.
ii. Levels of ADAMTS13 often normal.
d. Therapy.
i. Supportive care.
ii. Value of plasma exchange uncertain, but may be performed for severe cases.
TABLE 92-1 Drug-Induced Hemolytic Anemia | |||||||||||||||||||||||||||||||||
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