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ACUTE CHEST SYNDROME

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ACUTE CHEST SYNDROME Dr.Padma Gadde Dr. Dora Alvarez ACUTE CHEST SYNDROME Acute chest syndrome – PowerPoint PPT presentation

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Title: ACUTE CHEST SYNDROME


1
ACUTE CHEST SYNDROME
  • Dr.Padma Gadde
  • Dr. Dora Alvarez

2
ACUTE CHEST SYNDROME
  • Acute chest syndrome" (ACS) broadly describes a
    disease
  • leading cause of death
  • second most common cause of hospitalization in
    patients with sickle cell disease

3
ACUTE CHEST SYNDROME
  • Its rapid clinical course, with or without fever,
    is characterized by chest pain, cough,
    progressive anemia, hypoxemia, and the presence
    of new pulmonary infiltrates on chest radiographs

4
Learning Objectives
  • To identify the causes of acute chest syndrome
    (ACS) in patients with sickle cell disease
  • To understand the pathophysiology of ACS
  • To recognize elements that are important in
    appropriate management of ACS

5
ACUTE CHEST SYNDROME
  • The approach to diagnosis, monitoring, and
    treatment requires
  • recognition of the complication,
  • correction, if possible, of inciting factors,
  • maintenance of euvolemia,
  • pain control, and
  • use of transfusions and
  • administration of oxygen, if needed.

6
ACUTE CHEST SYNDROMERisk factors
  • Younger age
  • Homozygous sickle cell or sickle cell-beta
    thalassemia genotype
  • Winter months
  • Fever

7
ACUTE CHEST SYNDROMERisk factors
  • Surgery
  • Avascular necrosis of bone
  • Previous pulmonary events
  • High hemoglobin levels
  • High steady-state leukocyte counts
  • Low fetal hemoglobin concentration

8
Pathophysiology
  • The pathogenesis of parenchymal lung infiltrates
    in ACS is incompletely understood.
  • Pulmonary infiltrates may result from either one
    process or a combination of several interacting
    processes, which may include
  • atelectasis,
  • infection,
  • fat embolism,
  • thromboembolism and,
  • most commonly, in situ microvascular occlusion
    within the pulmonary vasculature by sickled
    erythrocytes

9
Pathophysiology
  • The importance of nonembolic microvascular
    occlusion in causing ACS is demonstrated by
    findings on thin-cut computed tomographic scans
    Arterioles and venules are either absent or
    diminished in number, and ground-glass opacities
    appear in a mosaic, patchy, or multifocal
    distribution

10
pathophysiology
  • Fat embolism from bone marrow necrosis seems to
    be an important and often unrecognized cause of
    ACS

11
pathophysiology
  • Patients with pulmonary fat embolism are more
    likely than others to have severe bone and chest
    pain, changes in mental status, and a prolonged
    hospital course.
  • A complete blood cell count in these patients
    shows more severe anemia and thrombocytopenia
    than in patients without pulmonary fat embolism,
    and chest radiographs reveal more multilobar
    infiltrates

12
pathophysiology
  • sPLA2 liberates free fatty acids from
    phospholipids.
  • Measurement of secretory phospholipase A2 (sPLA2)
    levels may be helpful, because they have recently
    been found to be elevated in patients with sickle
    cell disease and ACS from pulmonary fat embolism

13
pathophysiology
  • An early rise in these levels precedes the
    development of ACS and thus may be a useful
    marker in predicting its occurrence.
  • Furthermore, sPLA2 levels correlate with disease
    severity.

14
Mechanisms of hypoxemia
  • Hypoventilation due to
  • Direct chest-wall splinting from either rib and
    sternal infarctions or abdominal crisis
  • Excessive sedation from narcotic analgesics,
    leading to decreased oxygen exchange

15
Mechanisms of hypoxemia
  • Ventilation-perfusion mismatch possibly caused by
    diseases that underlie or result from acute chest
    syndrome
  • Pneumonia
  • Mucous plugging
  • Aspiration
  • Bronchospasm
  • Pulmonary hypertension
  • Cor pulmonale

16
Mechanisms of hypoxemia
  • Impaired oxygen diffusion from repetitive
    episodes of acute chest syndrome that ultimately
    result in restrictive lung disease (2,3)

17
Evaluation
  • ACS is more severe in adolescents and adults than
    in children.
  • Patients most commonly present with shortness of
    breath, chills, and pleuritic chest pain, but no
    fever

18
Evaluation
  • In some cases, physical signs of disease are
    delayed and are first noted during
    hospitalization.

19
Evaluation
  • These include
  • chest-wall tenderness secondary to rib
    infarction.
  • dullness to percussion caused by pleural
    effusion.
  • and auscultatory rales from pulmonary
    consolidation.

20
Evaluation
  • Results of laboratory studies may show
  • anemia with thrombocytopenia
  • or thrombocytosis,
  • leukocytosis,
  • and evidence of hemolysis,
  • including elevated LDH
  • bilirubin levels

21
Evaluation
  • Findings on chest radiographs, although not
    pathognomonic, include
  • patchy lower-lobe involvement in a segmental,
    lobar, or multilobar distribution, with or
    without pleural effusion.
  • Correlation between the extent of consolidation
    found on chest radiographs and the severity of
    hypoxemia is poor

22
Evaluation
  • The presence of bilateral pulmonary infiltrates,
    however, identifies a subset of patients who are
    more likely to have serious illness.
  • Their clinical course is characterized by
    tachycardia, protracted hypoxemia, longer
    duration of fever, and a greater fall in
    hemoglobin levels

23
Diagnostic tests for acute chest syndrome
  • Sputum analysis for Gram's stain
  • Blood cultures
  • Chest radiographs
  • Thin-cut computed tomographic scan of chest
  • Serial measurement of arterial blood gases
  • Ultrasound or impedance plethysmography
  • Bone scan
  • Flexible bronchoscopy with bronchoalveolar lavage

24
Management of acute chest syndrome in patients
with sickle cell disease
  • Identify and treat all underlying precipitating
    factors
  • Maintain adequate oxygenation, improve
    oxygen-carrying capacity, and improve tissue
    oxygen deliveryAdminister supplemental oxygen to
    maintain PaO2 in 70-100 mm Hg range

25
Management of acute chest syndrome in patients
with sickle cell disease
  • Give simple or exchange transfusion to enhance
    oxygen capacity or reduce hemoglobin S
    concentration to reverse episodes
  • For severe respiratory failure, use mechanical
    ventilation with positive end-expiratory pressure
    (PEEP) or continuous positive airway pressure
    (CPAP

26
Management of acute chest syndrome in patients
with SSD
  • Prevent further alveolar collapse by using
    incentive spirometry, CPAP, and PEEP
  • Maintain adequate fluid volumeGive hypotonic
    saline (D5W or 5 dextrose in 0.25 normal
    saline) to maintain normovolemic state

27
Management of acute chest syndrome in patients
with SSD
  • Control painGive adequate amounts of narcotic
    analgesics to alleviate pain, avoiding
    hypoventilation from excessive sedation
  • Nonsteroidal anti-inflammatory medications (if
    not contraindicated by underlying peptic ulcer or
    renal disease)
  • Morphine sulfate, 0.1-0.15 mg/kg every 3-4 hours
    intravenously, through fixed scheduling or
    patient-controlled analgesia

28
Management of acute chest syndrome in patients
with SSD
  • Treat underlying infectionProvide empirical
    coverage for community-acquired pneumonia,
    pending results from other studies use second-
    or third-generation cephalosporin or selected
    beta-lactam/beta-lactamase inhibitor in
    combination with macrolide
  • Prescribe bronchodilatorUse albuterol (Airet,
    Proventil, Ventolin) through metered-dose inhaler
    or nebulizer

29
Management of acute chest syndrome in patients
with SSD
  • Fluid administrationIf the patient is unable to
    consume fluids orally, 5 dextrose in water or 5
    dextrose in 0.25 normal saline solution should
    be administered intravenously to maintain
    euvolemia once any existing volume deficits have
    been corrected.

30
Management of acute chest syndrome in patients
with SSD
  • Dehydration must be remedied, because it can
    result in increased plasma osmolarity and
    intracellular dehydration of red blood cells.
  • Under those conditions, erythrocytes are more
    likely to sickle. Hypotonic saline solutions are
    used because free water enters the relatively
    hypertonic red blood cells.
  • This process causes osmotic swelling, decreased
    mean corpuscular hemoglobin concentration and,
    consequently, a reduced tendency for sickling.

31
Management of acute chest syndrome in patients
with SSD
  • Decisions regarding transfusion are best guided
    by the patient's clinical condition.
  • Simple transfusion is indicated for patients with
    mild to moderate ACS the goal is a hemoglobin
    value of 10 g/dL
  • Exchange transfusions should be reserved for
    severe crises, when it is important to decrease
    the hemoglobin S concentration rapidly.
  • Unlike simple transfusions, exchange transfusions
    avoid the problems related to increased blood
    volume and viscosity. It is suggested that a PaO2
    of less than 60 mm Hg, clinical deterioration, or
    a worsening condition seen on chest radiographs
    should prompt exchange transfusion.

32
Management of acute chest syndrome in patients
with SSD
  • The goal is to reduce the hemoglobin S
    concentration to 20 to 30 and the hematocrit to
    30 (5). Patients with recurrent episodes of ACS
    may also benefit from regular exchange
    transfusions to maintain the hemoglobin S
    concentration below 30.

33
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