Transcript Anemia

Anemia
Robb Friedman, MD
Modified by Sean Hesselbacher, MD,
Eyal Oren, MD, David Antonetti, MD
and Cathy Okuliar, MD
What is Anemia?
ANEMIA IS NEVER NORMAL
 Reduction below normal in the mass of
red blood cells in the circulation
 Hemoglobin concentration, hematocrit,
RBC count
 Men: HGB < 14 or HCT < 41%
 Women: HGB < 12.0 or HCT < 36%
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Anemia and Volume Status
HGB and HCT are CONCENTRATIONS
 Therefore dependent upon plasma volume
 Acute bleeds not reflected for 24-36 hrs
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– Due to volume deficit being slowly repaired via
movement of fluid from extravascular space to
intravascular
Anemic patients who are dehydrated will not
appear anemic
 Pregnant women expand RBCs 25% but plasma
volume increases 50%, producing “physiologic
anemia”
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Anemia: Special Cases
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Erythrocytosis
– People who live at high altitude have greater RBC
volume
– Smokers have increased HCT – impairs the ability of
the RBCs to deliver O2
African-American HGBs are 0.5 to 1.0g/dL lower
than Caucasians
 Athletes (increased plasma volume, Fe
deficiency, hemolysis, polycythemia, use of
performance enhancing agents)
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Anemia and the Elderly
Multiple studies show that the elderly do
not have a “lower normal range”
 Anemia, while common in the elderly, is
still abnormal
 HGB < 13 in males and < 12 in females
associated with an increased relative risk
of mortality (1.6 and 2.3 respectively)
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Anemia: History
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Is the patient bleeding?
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NSAIDs, ASA
Menstrual history, if applicable (include older women)
Prior intestinal surgery?
Hx of hemorrhoids, hematochezia, or melena?
Past medical history of anemia? Family history?
Alcohol, nutritional questions
Liver, renal diseases
Ethnicity
Environmental/work toxins (ie lead)
Symptoms of Anemia
Decreased O2 delivery
 Hypovolemia if acute loss
 Exertional dyspnea, fatigue, palpitations,
lightheadedness
 Severe: heart failure, angina
 “Pica”– craving for clay or paper products
 Pagophagia– craving for ice
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Signs of Anemia
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Tachycardia, tachypnea, orthostasis
Pallor
Jaundice
Murmur
Koilonychia or “Spoon nails”
Splenomegaly, lymphadenopathy
Petechiae, ecchymoses
Atrophy of tongue papillae
Heme + stool
The Four Causes of Anemia
 Decreased
red blood cell
production
 Increased red blood cell
destruction
 Red blood cell loss
 Red blood cell sequestration
* Underlying disorder is abnormal production vs. premature loss
Decreased RBC production
Deficiency of iron, B12, folate
 Marrow is dysfunctional from
myelodysplasia, tumor infiltration, aplastic
anemia, etc.
 Bone marrow is suppressed by
chemotherapy or radiation
 Low levels of erythropoeitin, thyroid
hormone, or androgens
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Increased RBC destruction
RBCs live about 100 days
 Acquired: autoimmune hemolytic anemia,
TTP-HUS, DIC, malaria
 Inherited: spherocytosis, sickle cell,
thalassemia
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RBC Loss
Bleeding!
 Obvious vs occult
 Iatrogenic: venesection e.g. daily CBC,
surgical, hemodialysis
 Retroperitoneal
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Approach to Anemia
CBC
Reticulocyte count
MCV
RI > 2%
RI < 2%
Underproduction
Increased destruction or loss
MCV
MCV < 80
Microcytic
MCV 81 – 99
Normocytic
MCV > 100
Macrocytic
Further work up
Based on history,
Physical, other
Approach to Anemia
LOOK AT THE
SMEAR!!!!
 Convenient to separate
into three classes based
on the size of the RBC
 MCV and RDW
 Microcytosis: < 80 fL
 Normocytosis: 80-100 fL
 Macrocytosis: >100 fL
 CBC, reticulocyte count,
Fe, Ferritin, TIBC, folate,
B12, LDH, CMP, ESR…
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Reticulocytes
Nucleated RBCs – form in marrow where they
mature for 3 days and then spend 1 day in
circulation (before maturing to RBC)
 Given avg life span of RBC of 100 days, 1% of
RBCs are destroyed each day
 Retics form 1% of circulating RBCs qd
 Nl RBC count is 5 million/uL so marrow makes
50,000 reticulocytes/uL blood qd
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– With epo, can increase to 250,000 retics/uL blood qd
(given nl marrow and replete iron, folate, b12)
Reticulocyte Count
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Assess adequacy of bone marrow response to anemia
Must adjust for the degree of anemia, use Reticulocyte
Production Index
RI = (measured retic) x (Hct/45) / (Correction Factor)
– CF: Hct 41-50 (1); 30-40 (1.5); 20-29 (2); 10-19 (2.5)
– Reflects increased circulating time for retics as Epo pushes them out
of the marrow earlier
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RI < 1.0 is abnormally low and indicates inadequate marrow
response
Microcytic Anemia
Iron Deficiency
Anemia
 Thallasemia
 Anemia of chronic
disease
 Sideroblastic anemia
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Iron Deficiency Anemia
The definitive test is serum ferritin
 Low serum ferritin (<12 ug/L)is
diagnostic of iron deficiency
 Although ferritin is an acute phase
reactant, it will still be low in iron
deficiency
 Also, high TIBC
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– Fe saturation = Fe/TIBC < 10% in
Fe deficiency
– If ferritin is indeterminate
Low serum Fe is not in itself
diagnostic, neither is marrow
staining
 Anisocytosis (heterogeneous in
shape) and poikilocytosis
(abnormal shape)
 Reactive thrombocytosis
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Iron deficiency
Thalassemia
Decreased production of either α-globin or
β-globin chains
 Abnormal hemoglobin electrophoresis
 Polychromasia (dark staining retics),
target cells, basophilic stippling
 Normal/increased RBC mass
 Mentzer index: MCV/RBC ct < 13
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Alpha-Thalassemia
Alpha-Thalassemia: 4 genes
 1/4: silent carrier
 2/4: Alpha-Thalassemia trait, microcytosis
and mild anemia
 3/4: excess Beta-chains form tetramers,
results in severe anemia and microcytosis
 4/4: hydrops fetalis
 Most common in SE Asian populations
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Basophilic stippling
Beta-Thalassemia
2 genes
 1/2 mutation: Beta-Thal trait, increased
Hgb A2, rarely anemic, mild microcytosis
 2/2 mutation: Beta-Thalassemia disease,
Hgb F, microcytosis, anemia
 Usually found in people of African or
Mediterranean descent but has world-wide
distribution
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Beta - Thalassemia
Sideroblastic Anemia
 Failure of synthesis of
porphyrin ring
Hereditary
 Acquired (INH, EtOH, B6
deficiency, Lead)
 Smear: sideroblasts and
basophilic stippling
Macrocytic Anemia (MCV>100)
Drug Induced (hydroxyurea, AZT, MTX,
chemotherapy, anticonvulsants)
 B12 / folate deficiency
 Myelodysplastic syndrome
 Liver disease
 Alcohol abuse
 Reticulocytes
 Hypothyroidism
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Folate and B12
Serum folate usually sufficient, but if folate level
is normal but folate deficiency is suspected,
check serum homocysteine (elevated because of
impaired folate dependent conversion of
homocysteine to methionine) or RBC-folate.
 B12 can be spuriously low– a more sensitive and
specific test is serum methylmalonic acid level,
will be increased if B12 is low.
 Classically check Schilling Test for B12 deficiency
(parietal cell antibody or Intrinsic Factor
antibody)
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B12 and Folate Deficiency
Myelodysplastic Syndrome
Primary bone marrow
disorder, often found
in elderly
 Macrocytosis, anemia
 Pseudo-Pelger-Huet
abnormality– the
bilobed nucleus
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Normocytic Anemia
Large and complicated group of disorders!
 Hemolytic anemias
 Anemia of chronic disease
 Bone marrow disorder
 Nutritional (early Fe, B12, folate
deficiency)
 Renal insufficiency
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Nutritional Anemias
Iron deficiency and B12/folate deficiency
can present with normocytic anemia– esp.
if both deficiencies are concurrent.
 Check iron studies and B12, folate levels.
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Anemia of Renal Insufficiency
Unremarkable peripheral blood smear
 Inappropriately normal erythropoietin level
 Anemia usually severe and symptomatic
when Cr > 3.0
 Mild to moderate anemia found in Cr 1.53.0
 Tx: Epogen or similar, Fe (oral, IV) if iron
stores are found to be low
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Hemolytic Anemias
Evaluation of Hemolysis
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LDH: increases
Indirect bilirubin increases
(increased Hgb catabolism)
Haptoglobin decreases
Reticulocyte count increases
Urine hemosiderin test =
present in intravascular,
absent in extravascular
hemolysis!
Coombs test:
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(+) = autoimmune hemolytic
anemia
– (-) consider PNH (abnormal
GPI protein, send flow for
CD55 and CD59)
Hemolytic Anemia: Intrinsic causes
Spherocytosis, Sickle Cell
More hemolytic anemias
Anemia of Chronic Disease
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Thought to be a cytokine mediated process
which inhibits red blood cell production or
interferes with action of erythropoietin
– Therefore, the disease needs to be inflammatory
Decreased iron utilization/mobilization
 Seen with rheumatologic diseases, chronic
infections, malignancy
 Indices: Low Fe, Low TIBC, Nl/increased Ferritin
 May be seen in conjunction with Fe-deficiency
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Anemia due to Primary Bone
Marrow Disorder
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Myelodysplastic syndrome
Bone marrow infiltration:
nucleated red blood cells
found in circulation
Might see “rouleaux”
formation in multiple
myeloma
WBC, plts often abnormal
Bone marrow biopsy
Anemia: Treatments
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“Transfusion triggers”
– CAD: Hgb > 10
– All pts: Hgb > 7.0
Iron supplementation
 Erythropoietin analogs
 B12, folate
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What in the world is a Howell-Jolly
Body?
Acanthocytes vs Echinocytes
Acanthocytes: “spur cells” found in liver disease
 Echinocytes: “burr cells” found in renal disease
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Helmet vs. Teardrop Cells
Anemia: Summary
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ANEMIA IS NEVER NORMAL
Determine if ACUTE or CHRONIC
CONSIDER THE FOUR CAUSES
CALCULATE the RETIC INDEX
LOOK AT THE SMEAR
CONSIDER THE ETIOLOGY BASED ON RBC
MORPHOLOGY AND LABORATORY STUDIES
TREAT APPROPRIATELY
MKSAP Questions
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An 80-year-old man who had a hemicolectomy for colon cancer is
evaluated because of a 4-month history of diarrhea, anorexia, and
fatigue. He had a remote history of alcoholism.
On physical examination, he is cachectic and mildly confused. His
pulse rate is 70/min, and blood pressure is 140/85 mm Hg. His
tongue is smooth. The abdomen is soft; there are no palpable
masses or hepatosplenomegaly. A stool specimen is negative for
occult blood. Neurologic examination shows loss of position sense in
the feet. He has a wide-based gait. The Romberg test is positive. His
hemoglobin is 9.4 g/dL, reticulocyte count is 2.5%, mean
corpuscular volume is 125 fL, and serum lactate dehydrogenase is
400 U/L.
Which of the following is the most likely cause for his
symptoms?
( A ) Alcoholic cerebellar degeneration
( B ) Vitamin B12 deficiency
( C ) Brain metastases
( D ) Folate deficiency
( E ) Liver metastases
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Critique (Correct Answer = B)
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The patient most likely has vitamin B12 deficiency, based on the degree of macrocytosis and neurologic
findings. An elevated serum lactate dehydrogenase level, due to intramarrow cell death from ineffective
erythropoiesis, is consistent with this diagnosis.
Severe macrocytosis (mean corpuscular volume > 120 fL) is often associated with vitamin B12 deficiency or
folate deficiency (megaloblastic anemia), usually seen in conjunction with “oval” macrocytes. The presence o
frequent hypersegmented neutrophils (> 5 segments) is strongly suggestive of vitamin B12 or folate
deficiency.
Bone marrow morphology in patients with vitamin B12 or folate deficiency is referred to as “megaloblastic”
and is characterized by the presence of large cells with immature nuclear chromatin but maturing erythrocyt
cytoplasm (nuclear-cytoplasmic dissociation). Anemia accompanies this process; hence the term “ineffective
erythropoiesis.” The intramarrow death of megaloblastic cells causes the serum lactate dehydrogenase level
to rise. If a patient has a low serum vitamin B12 or folate level, a bone marrow examination is probably
unnecessary. However, the physician should determine the cause of the deficiency. If a patient has a normal
serum vitamin B12 or folate level, a bone marrow examination is frequently helpful to exclude
myelodysplastic syndromes or other infiltrative marrow disorders.
Folate deficiency can induce megaloblastosis within weeks to months, whereas vitamin B12 deficiency
requires years to cause megaloblastosis since stores of vitamin B12 persist for years in the liver and other
tissues. In patients with vitamin B12 or folate deficiency, parenteral or oral repletion of vitamin B12 or folate
reverses some morphologic abnormalities within hours. Serum folate levels fluctuate quickly with changes in
dietary consumption. Low erythrocyte folate levels often reflect prior nutritional depletion. In patients who
are hospitalized and are begun on regular diets, the erythrocyte folate test may provide a better assessment
of tissue folate levels than determination of the serum folate level. The erythrocyte folate test often requires
a special laboratory, and results often are not quickly available.
In patients with megaloblastic anemias, erythrocyte production is diminished and a “corrected” reticulocyte
count is inappropriately low for the degree of anemia. This patient had a corrected reticulocyte count of 1%
(inappropriately low for a hemoglobin level of 9.4 g/dL).
In addition to changes in the blood, the epithelial cells in patients with megaloblastic anemias may become
atrophic and cause a smooth tongue and cheilosis. Posterior column dysfunction, particularly in patients with
vitamin B12 deficiency, may lead to changes in vibratory or position sense, causing ataxia. Signs of dementia
may appear. However, neurologic dysfunction is very uncommon in adults with folate deficiency.
Alcoholic cerebellar degeneration results in ataxia but not position loss. Although liver metastases are
possible in a patient with a history of colon cancer, their presence would not account for the neurological
findings in this patient. Brain metastases would most likely produce focal neurological findings and also woul
not account for the blood findings.
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A 26-year-old man is evaluated because of progressive fatigue,
dyspnea on exertion, and orthostatic dizziness for the past 2 to 3
weeks. He takes no medications. Physical examination is normal
except for pallor.
Laboratory Studies: Hematocrit 13%Leukocyte count 8300/μL;
normal differential. Reticulocyte count: 0, Platelet count 320,000/μL.
A routine biochemical profile, including liver function tests, is
normal. A chest radiograph shows normal lung fields and a widened
mediastinum, suggestive of an anterior mediastinal mass. Bone
marrow biopsy shows absent erythrocyte precursors, normal
megakaryocytes, and normal leukocyte numbers and maturation.
Which of the following is the most likely cause of the
mediastinal mass and anemia?
( A ) Hodgkin’s disease
( B ) Non-Hodgkin’s lymphoma
( C ) Thyroid carcinoma
( D ) Thymoma
( E ) Germ cell carcinoma
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Critique (Correct Answer = D)
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Each of the listed neoplasms may present as an anterior
mediastinal mass and may be associated with anemia of
chronic disease. However, pure red cell aplasia (which this
patient has) is often associated with a benign or invasive
thymoma. Approximately 5% to 15% of thymomas occur in
patients with pure red cell aplasia. Other thymoma-associated
autoimmune disorders include myasthenia gravis, systemic
lupus erythematosus, thrombocytopenia, and, rarely,
malabsorption states. A careful search by CT or MRI is always
warranted in patients with newly diagnosed or relapsing red cell
aplasia or myasthenia.
The other listed entities are also included in the differential
diagnosis for an anterior mediastinal mass. Germ cell tumors
have not been associated with pure red cell aplasia, and
Hodgkin’s disease, non-Hodgkin’s lymphoma, and thyroid
carcinoma are rarely associated with this disorder. Chronic
lymphocytic leukemia is also commonly associated with red cell
aplasia and may present with variable degrees of
lymphadenopathy but not with an isolated anterior mediastinal
mass, as in the patient discussed here.
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A 36-year-old black man with known sickle cell anemia is evaluated
because of a 2-week history of fever, a macular rash on his trunk,
and arthralgias. Subsequently, he developed weakness and dyspnea
on exertion. Several of his children had febrile illnesses with
associated rashes and fatigue over the past month. These illnesses
resolved spontaneously without sequelae.
On physical examination, his temperature is 38.8 °C (101.8 °F),
pulse rate is 100/min, and blood pressure is 160/70 mm Hg. A
maculopapular, truncal rash is noted. There is conjunctival pallor.
The remainder of his examination is unremarkable.
Laboratory StudiesHemoglobin 5.2 g/dLLeukocyte count
5000/μLReticulocyte count 0%Platelet count 130,000/μLSerum
lactate dehydrogenase 622 U/LWhich of the following is the
most likely diagnosis?
( A ) Paroxysmal nocturnal hemoglobinuria
( B ) Parvovirus infection
( C ) Glucose-6-phosphate dehydrogenase deficiency
( D ) Aplastic anemia
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Critique (Correct Answer = B)
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Patients with hemolytic disorders may occasionally present with reticulocytopenia and an “aplastic crisis.” This
patient has sickle cell anemia with parvovirus infection, which is causing an aplastic crisis. Parvovirus may
infect patients with hemolytic anemias (for example, patients with hereditary spherocytosis, sickle cell
disease, or thalassemia). In children with sickle cell anemia, over 80% of aplastic crises may be attributed to
parvovirus infections. In adults, the usual presenting features are rash, arthritis, and anemia. The “slapped
cheek” syndrome is rarely a presenting feature. There is usually a complete suppression of erythropoiesis to
a reticulocyte level of 0%. The bone marrow shows giant dysplastic (megaloblastoid) erythroblasts,
occasionally with viral inclusions. The diagnosis is usually made by demonstrating IgM antibodies to the virus.
IgG antibodies appear later during the course of the infection and persist. Parvovirus in the blood may be
detected by the polymerase chain reaction, which is the definitive diagnostic method. Occasionally, other
blood components such as leukocytes and platelets are affected and result in mild to moderate pancytopenia.
The diagnosis of paroxysmal nocturnal hemoglobinuria (PNH) should be considered in patients with bone
marrow failure or aplasia, unusual location of thromboses, and unexplained hemolysis. The anemia may be
severe, and patients with PNH typically have reticulocytopenia. There is no characteristic finding on bone
marrow examination, although the bone marrow of patients with PNH may demonstrate myelodysplastic
changes. The diagnosis is based on demonstration of exquisite sensitivity to complement-mediated lysis by
the sucrose lysis test or the acidified serum lysis test (Ham’s test).
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is another cause of hemolysis that occasionally is
associated with reticulocytopenia. In patients with G6PD deficiency, erythrocytes are subject to oxidative
stresses. Hemoglobin becomes oxidized and precipitates within the erythrocytes, which then undergo
destruction by the reticuloendothelial system. G6PD deficiency is an autosomal recessive disorder that
predominantly affects males. After a hemolytic episode, qualitative assays may be normal because only
erythrocytes that are resistant to G6PD remain. The African variant of G6PD is associated with a mild form of
hemolysis, whereas the Mediterranean variant is usually severe. Causes include infectious stresses, drugs
such as quinidine and sulfonamides, or, in the Mediterranean variant, favism (consumption of fava beans).
Therapy requires avoiding certain medications and supportive care in crisis situations.
In contrast to this patient’s presentation, patients with aplastic anemia have pancytopenia with severe
anemia, reticulocytopenia, thrombocytopenia, and granulocytopenia. In patients with severe aplastic anemia,
the bone marrow examination shows less than 5% cellularity with only residual lymphocytes and plasma
cells. The abnormal cells described above that are attributable to parvovirus infection are not seen.
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A 36-year-old man is evaluated because of fatigue. He has had two
episodes of acute gouty arthritis over the past 6 months. He has a 10-year
history of significant alcohol use, but he quit drinking 4 months ago. He
works in a factory making battery products. A complete blood count
obtained prior to elective hernia repair surgery 4 years ago was normal. He
takes no medications.
On physical examination, his temperature is 37.3 °C (99.1 °F), pulse is
60/min, and blood pressure is 135/70 mm Hg. His skin is normal. There is
slight scleral icterus. There is a blue line at the edge of his gums.
The remainder of the examination is normal. Stool specimens are negative
for blood on three occasions.
Laboratory StudiesHemoglobin 7.5 g/dLMean corpuscular volume 71
flLeukocyte count 9400/µLReticulocyte count 5.3%Platelet count
435,000/µLSerum lactate dehydrogenase 553 U/LSerum uric acid 11
mg/dLA peripheral blood smear is shown.
Which of the following diagnostic studies is most useful for
determining the cause of this patient’s anemia?
( A ) Serum iron, total iron-binding capacity, and ferritin levels
( B ) Serum lead levels
( C ) Direct and indirect antiglobulin tests
( D ) Hemoglobin A2 quantitation
( E ) Serum ethanol and folic acid levels
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Critique (Correct Answer = B)
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The patient has chronic lead intoxication that can be confirmed by measuring serum lead levels.
He has a hypochromic, microcytic anemia with coarse basophilic stippling and reticulocytosis.
He also has evidence of hemolytic anemia with increased serum lactate dehydrogenase and
indirect bilirubin levels. His physical examination is remarkable for gingival “lead lines.” Bone
marrow examination shows erythroid hyperplasia and ringed sideroblasts. The anemia of lead
poisoning fits this description. Sideroblastic anemia with hypochromic indices is typical.
Hemolysis is common, and basophilic stippling, blue staining polyribosomal aggregates with
mitochondrial fragments in the erythrocytes, is frequently seen. Lead inhibits pyrimidine 5′nucleotidase which normally clears ribosomal fragments. Occupational exposures to lead are
relatively uncommon today. However, workers who produce batteries or are exposed to paint,
particularly those who remove leaded paint from old buildings, are at greatest risk if they are
not protected from inhalation of paint particles during the sanding process. Other
manifestations of lead toxicity in adults include peripheral neuropathy, abdominal colic, and
saturnine gout (effects of lead on renal tubules that prevent the excretion of uric acid).
Chelation therapy is indicated for patients with serum lead levels exceeding 70 µg/dL and
should be continued until lead levels fall below 40 µg/dL. Agents such as EDTA or dimercaprol
may also be effective.
This patient is unlikely to have iron deficiency since his reticulocytes are increased. In addition,
basophilic stippling usually is not seen in patients with iron deficiency.
Thalassemia is associated with a microcytic anemia, reticulocytosis, and basophilic stippling.
However, a normal complete blood count 4 years ago rules out this possibility. Therefore,
quantitative studies to measure hemoglobin A2 are not necessary.
Autoimmune hemolytic anemia should be excluded by performing a direct antiglobulin test in
any patient who has evidence of hemolysis on a peripheral blood smear. However, the “lead
lines” on this patient’s gingivae are classic for lead poisoning, and autoimmune hemolytic
anemia therefore is less likely.
Alcoholism may cause a transient sideroblastic anemia, which resolves with cessation of alcohol
intake. Folic acid deficiency may complicate alcoholism but usually presents with macrocytosis.
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A 22-year-old man is evaluated in the intensive care unit because of
bleeding immediately after scoliosis surgery. During surgery, 12
units of packed red blood cells and 12 units of fresh frozen plasma
were transfused. There is no history of a bleeding disorder or of
drug administration that could affect platelet function.
On physical examination, the patient is afebrile. His pulse rate is
100/min, and blood pressure is 110/72 mm Hg. Petechiae are
present on his arms, and blood is oozing from the drains.
Laboratory StudiesHemoglobin 9.0 g/dLPlatelet count
43,000/µLProthrombin time 12 sActivated partial thromboplastin
time 32 sPlasma fibrinogen 400 g/dLd-Dimers NegativeWhich of
the following is the most likely cause of the
thrombocytopenia and bleeding?
( A ) Dilutional thrombocytopenia
( B ) Incompatible blood transfusion
( C ) Posttransfusion purpura
( D ) Septic transfusion reaction
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Critique (Correct Answer = A)
Approximately a 50% reduction in the platelet count occurs when
transfusions of 1.5 to 2 times the blood volume are given over 4 to 8 hours.
Blood stored for more that 2 to 3 days has essentially no platelets, which
explains the thrombocytopenia. Fresh frozen plasma contains all of the
clotting proteins in normal concentrations. This patient received one unit of
fresh frozen plasma for each unit of transfused red blood cells, which
resulted in no measurable alteration in the prothrombin time or activated
partial thromboplastin time. Incompatible red blood cell transfusions can
lead to the development of disseminated intravascular coagulation, which is
characterized by thrombocytopenia. The other hallmarks of disseminated
intravascular coagulation are absent in this patient, namely, he has a
normal fibrinogen, prothrombin time, activated partial thromboplastin time,
and negative d-dimers. Posttransfusion purpura is characterized by
profound thrombocytopenia that develops 5 to 7 days after a transfusion. It
occurs in patients who are negative for the PLA-1 human platelet antigen
and have been transfused or pregnant in the past. Posttransfusion purpura
almost always occurs in women.
 Septic transfusion reactions can be associated with thrombocytopenia when
either bacteremia or endotoxemia causes disseminated intravascular
coagulation. This patient has no indication of either sepsis or disseminated
intravascular coagulation.
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