Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3055_Библиотеки_им_академика_М_И_Перельмана.pdf
278
Able to exercise
Yes
Normal ECG
Exercise stress
with or without
imaging
ECHO stress
test with or
without imaging
pharmacologic
stress testing
with myocardial
imaging
stress
echocardiography
or stress
radionuclide
myocardial
perfusion imaging
Normal ECGAbnormal EC
GA
bnormal ECG
No
Fig. 16.3 Approach to choosing the optimal stress test
Table 16.4 Sensitivity and specificity for detecting coronary artery
disease
Test Sensitivity (%) Specificity (%)
Exercise treadmill ECG test 45–61 70–90
Exercise nuclear perfusion
imaging
73–92 63–88
Dobutamine stress myocardial
perfusion imaging
88–91 75–90
Exercise echocardiography 70–85 77–89
Dobutamine stress
echocardiography
72–90 79–95
Coronary CTA
(not widely used)
93–90 64–90
Adapted from Heart Int. 2012; 7(1):e2. [6]
CTA computed tomography angiogram
• Preoperative evaluation for non-cardiac surgery in patients
deemed to be at high risk [5]
• Treatment
M.M. Amer
279
Unstable Angina
In patients with chest pain with or without new ECG
changes (ST or Q waves) and high to moderate cardiac risk
(Table 16.2), give aspirin 162–325 mg by mouth, oxygen,
and NTG, obtain IV access, do cardiac monitoring and
blood work which includes cardiac enzymes, and refer to
the ER. Patients with chest pain and no ECG changes and
low cardiac risk may be referred for outpatient stress test-
ing. See Fig. 16.4.
Stable Angina
In patients with stable ischemic heart disease, the first-line
therapy to reduce anginal episodes and improve exercise tol-
erance is beta-blockers. Furthermore, beta-blockers are the
only antianginal medication shown to prevent reinfarction
Cardiac chest
pain
ECG + ischemic
changes
Yes
O2, ASA, NTG
High Risk
Table 1
Low Risk
Stress test
Positive
Cardiology
referral
Non-cardiac
cause
Negative
No
Fig. 16.4 Clinical approach for cardiac chest pain
16. Chest Pain
280
and to improve survival in patients who have already had a
myocardial infarction [7].
Nitrates should be used for relief of acute anginal symp-
toms, and they may also help to prevent recurrent angina
episodes through coronary vasodilation.
All patients should be treated with aspirin in doses from
75 to 325 mg provided there is no contraindication to anti-
platelet therapy.
Ranolazine, a piperazine derivative, was approved by the
FDA in 2006 as a new antianginal agent to treat chronic sta-
ble angina. It is intended for use as combination therapy
when angina is not adequately controlled with other antiangi-
nal agents [8].
The following patients should be referred to the emer-
gency room:
• Aortic dissection: unequal blood pressures bilaterally
• Pneumonia: fever and cough, infiltrates on chest X-ray,
Curb 65 score ≥ 2
• Pneumothorax: decreased lung sounds unilaterally.
Changes in fremitus and percussion. Diagnosis made by
chest X-ray
• Pulmonary embolism: hemoptysis and dyspnea in a patient
with risk factors
Young patients with low cardiovascular risk presenting
with heartburn, and epigastric pain, may be sent home
with an antacid and followed up after 2–3 weeks. Patients
who have a low cardiovascular risk, are afebrile, and pres-
ent with localized pain and tenderness, may be managed
with NSAIDs and pain control for costochondritis. See
Fig. 16.5.
Clinical Pearls
• Comprehensive history and examination are vital to the
diagnosis.
• Consider the differential diagnosis when interpreting
symptoms and signs and investigating results.
• Evaluate risk factors for cardiac disease when assessing a
patient.
M.M. Amer
281
Non-cardiac
chest pain
Fever, cough,
sore throat,
runny nose
CXR reveals
infiltrates
Yes
CURB 65 2 or
more send to ER
CURB 65 0 or 1
oral antibiotics
No
control BP and
send to ER
pain
management
CT chest if
positve, send to
ER
Antacid, proton
pump inhibitor
send home with
follow up
BP measure
different in
both arms
Heartburn,
epigastric pain,
history of GERD
localized
tenderness
Hypoxia, history of
recent surgery,
recent trip,
malignancy,
immobility
Fig. 16.5 Clinical approach for noncardiac chest pain
16. Chest Pain
282
Don’t Miss This!
• If a patient is acutely unwell with chest pain and the cause
is not clear, err on the side of caution and send the patient
to ER for further assessment.
• Remember that women can present atypically with cardiac
ischemia that may mimic GI distress.
References
1. Sekhri N, Feder GS, Junghans C, et al. How effective are rapid
access chest pain clinics? Prognosis of incident angina and
non-cardiac chest pain in 8762 consecutive patients. Heart.
2007;93(4):458–63. Epub 2006 Jun 21
2. Shaw LJ, Bugiardini R, Bairey Merz CN. Women and isch-
emic heart disease: evolving knowledge. J Am Coll Cardiol N.
2009;54:1561–75.
3. Vaccarino V, et al. Sex-based differences in early mortality after
myocardial infarction. National Registry of Myocardial Infarction
2 Participants. N Engl J Med. 1999;341:217–25.
4. Stangl V, Witzel V, Baumann G, Stangl K. Current diagnostic
concepts to detect coronary artery disease in women. Eur Heart
J. 2008;29:707.
5. Miller TD. Exercise treadmill test: estimating cardiovascular
prognosis. Cleve Clin J Med. 2008;75:424.
6. Arbab-Zadeh A. Stress testing and non-invasive coronary angiog-
raphy in patients with suspected coronary artery disease: time for
a new paradigm. Heart Int. 2012;7(1):e2. https://doi.org/10.4081/
hi.2012.e2.
7. Fihn SD, Gardin JM, Abrams J, et al. 2012 ACCF/AHA/ACP/
AATS/PCNA/SCAI/STS guideline for the diagnosis and man-
agement of patients with stable ischemic heart disease: a report
of the American College of Cardiology Foundation/American
Heart Association task force on practice guidelines, and the
American College of Physicians, American Association for
Thoracic Surgery, Preventive Cardiovascular Nurses Association,
Society for Cardiovascular Angiography and Interventions, and
Society of Thoracic Surgeons. Circulation. 2012;126:e354.
8. Rayner-Hartley E, Sedlak T. Ranolazine: a contemporary review.
J Am Heart Assoc. 2016;5:e003196.
M.M. Amer
283© Springer International Publishing AG 2018
E. Sydney et al. (eds.), Handbook of Outpatient Medicine,
https://doi.org/10.1007/978-3-319-68379-9_17
Introduction
The diagnosis and initial evaluation of anemia is an important
aspect of the internist’s office practice. This chapter provides an
algorithm-based approach to help guide the internist through
the differential diagnoses and decision-making process.
Key History and Physical Exam
Primary care physicians should focus their evaluation toward
obtaining clues useful for accurate diagnosis of anemia and
its etiology. Key questions include the following: Any evidence
of blood loss? What is the duration of the anemia? Is this
Chapter 17
Anemia
Niraj K. Shenoy and Hernando J. Cordero
N.K. Shenoy, MD (*)
Department of Medicine (Hematology and Oncology),
Mayo Clinic, 200 First Street SW, Gonda Bldg, 10th floor,
Rochester, NY 55905, USA
e-mail: shenoy.niraj@mayo.edu
H.J. Cordero, MD
Department of Medicine, Jacobi Medical Center,
1400 Pelham Pkway S, Bronx, NY 10461, USA
e-mail: Hernando.Cordero@nbhn.net
284
genetic or acquired? Is infection or malignancy likely? Are
there associated features or comorbidities known to cause
anemia (e.g., renal failure, rheumatoid arthritis, and inflam-
matory bowel disease)? Does the patient’s ethnicity influ-
ence the differential? A careful review of medications,
including the use of aspirin and nonsteroidal anti-inflamma-
tory drugs, needs to be performed.
Classic symptoms that must be addressed include bleeding,
fatigue, fever, weight loss, night sweats, and signs of infection.
Physical examination can reveal tachycardia, hypotension
in acute blood loss, conjunctival pallor, jaundice, strong
peripheral pulses, systolic blood flow murmur, lymphade-
nopathy, hepatosplenomegaly, bone tenderness, petechiae,
and ecchymoses.
Diagnosis and Evaluation
• CBC (complete blood count) initial variables to review:
hemoglobin (Hgb), hematocrit (Hct), corpuscular volumes
[mean corpuscular volume (MCV), mean corpuscular
hemoglobin (MCH), mean corpuscular hemoglobin con-
centration (MCHC)], red blood cell (RBC) count, red cell
distribution width (RDW), platelet count, and white blood
cell (WBC) count with differential.
• Reticulocyte count to calculate the reticulocyte index and
determine the nature of the anemia: hypoproliferative or
hyperproliferative.
• Iron storage/supply [serum iron, total iron-binding capac-
ity (TIBC), serum ferritin].
• Abnormalities in direct and indirect bilirubin, lactate
dehydrogenase (LDH), and haptoglobin will suggest a
hemolytic process.
• Peripheral blood smear: detailed evaluation for evidence
of variations in cell size (anisocytosis) and cell shape
(poikilocytosis).
• In some patients more advanced testing, such as hemoglo-
bin electrophoresis and bone marrow examination (smear
and aspirate), is warranted (Fig. 17.1).
N.K. Shenoy and H.J. Cordero
285
Anemia
Hct < 41% or Hgb <13.5 ♂
Hct < 36% or Hgb <12.5 ♀
H&P
Reticulocyte Index (RI)
RI= [reticulocyte count x (Pt’s Hct /nl Hct)] / maturation factor]
**maturation factors: Hct: 45%: 1, 35%: 1.5, 25%: 2, 20%: 2.5
RI <2%
UNDERPRODUCTION
low MCV
MICROCYTIC
normal MCV
NORMOCYTIC
Marrow damage: Megaloblastic
üInfiltration, fibrosis
üFloate deficiency
üVit B12 deficiency
üDrug toxicity
Non-Megaloblastic
üAlcoholism
üHypothyroidism
üMDS
üRefractary anemia
üAnemia of Chronic
Inflammatinon
üMetabolic defect
üRenal disease
Iron deficiency
Decreased stimulation
üAplasia
High MCV
MACROCYTIC
RI >2%
INCREASED DESTRUCTION or LOSS
Elevated LDH, billirubin,
haptoglobin HEMOLYSIS
Signs and symptoms of bleeding
HEMORRHAGE
Iron deficiency
Thalassemia
Sideroblastic
Anemia of Chronic
Inflammatinon
Fig. 17.1 Anemia algorithm
17. A nemi a
286
Hypoproliferative Anemias
The reticulocyte index is <2% in hypoproliferative anemia.
Microcytic Anemias
These are characterized by smaller RBCs (MCV < 70) due to
decreased production of hemoglobin. Common causes are
lack of globin production (thalassemia), restricted iron deliv-
ery to the heme group (inflammation), lack of iron delivery
to the heme group (iron-deficiency anemia), and defects in
the synthesis of the heme group (sideroblastic anemia) [1].
Iron studies will guide us toward the most likely etiology, as
shown in the following Table 17.1.
Iron-Deficiency Anemia
Iron deficiency is the most common cause of anemia and is
estimated to be present in 1–2% of the adult population. Iron
deficiency in the absence of anemia is present in up to 11%
of the adult population [2]. Decreased marrow iron and
depleted iron stores cause decreased heme synthesis, leading
to microcytosis and anemia.
In addition to general anemia symptoms, specific iron defi-
ciency manifestations can include pica and pagophagia, brit-
tle integument, and restless leg syndrome.
Serum ferritin level is the most sensitive and specific test
used for the identification of iron deficiency (level of
<12 ng/mL). In those with combined inflammation and iron
deficiency, ferritin may be falsely elevated because it is an
acute-phase reactant. Soluble transferrin receptor is not
affected by inflammatory states and is a useful test to deter-
mine the presence of iron deficiency. If erythroid precursor
cells have cellular iron deficiency, they express increased
transferrin receptors to attract the iron-carrying transferrin.
Some of these transferrin receptors then spill out in the
N.K. Shenoy and H.J. Cordero
287
Table 17.1 Iron studies in microcytic anemia
Serum iron TIBC Transferrin saturation Serum ferritin
Normal range 40–180 ug/dL 205–450 ug/dL 25–35% 18–300 ng/mL
Iron deficiency Low < 40 ug/dL High > 350 ug/dL <15% Low <12 ng/mL
Anemia of chronic
disease
Low < 40 ug/dL Low < 300 ug/dL >15% Normal–high
Thalassemia Normal to high Normal to high Normal >30% Normal–high
Iron overload
(hemosiderosis)
High High >45% Increased
17. A nemi a