Download PowerPoint Sunusu

Adult Respiratory Distress
Syndrome
Prof.Dr Yaşar Küçükardalı
İç Hastalıkları ve Yoğun Bakım Uzmanı
• The age-adjusted incidence was 86 per 100,000
person-years for individuals with an arterial
oxygen tension to fraction of inspired oxygen
(PaO2/FiO2) ratio ≤300 mmHg and 64 per 100,000
person-years for individuals with a PaO2/FiO2
≤200 mmHg.
• ●The incidence increased with patient age from
16 per 100,000 person-years among individuals
15 to 19 years of age to 306 per 100,000 personyears among individuals 75 to 84 years of age.
definition
ARDS is an acute, diffuse, inflammatory lung
injury that leads to
• increased pulmonary vascular permeability,
• increased lung weight,
• a loss of aerated tissue
• Clinical hallmarks of ARDS are hypoxemia and
bilateral radiographic opacities,
• Pathological hallmark is diffuse alveolar damage
alveolar edema with or without focal hemorrhage
acute inflammation of the alveolar walls
hyaline membranes
Clinical presentation
• The clinical features of ARDS usually appear
within 6 to 72 hours of an inciting event and
worsen rapidly
• Patients typically present with dyspnea,
cyanosis (ie, hypoxemia), and diffuse crackles.
• Respiratory distress is usually evident,
including tachypnea, tachycardia, diaphoresis,
and use of accessory muscles of respiration.
• A cough and chest pain may also exist.
• Arterial blood gases reveal hypoxemia, which
is often accompanied by acute respiratory
alkalosis and an elevated alveolar-arterial
oxygen gradient
•
• High concentrations of supplemental oxygen
are generally required to maintain adequate
oxygenation.
A conservative estimate of normal A–a gradient is less than [age in years/4] + 4
• Clinical findings related to the precipitant may
also exist at presentation. As an example, in
patients with ARDS due to sepsis,
• there may be fever,
• hypotension,
• leukocytosis,
• lactic acidosis,
• disseminated intravascular coagulation (DIC).
Long Term
• Chronic
Respiratory
Disease
• Muscle Fatigue
• Muscle Wasting
• Weakness
• Clinical course — The first several days of ARDS are characterized by
hypoxemia requiring a moderate to high concentration of inspired oxygen.
The bilateral alveolar infiltrates and diffuse crackles are persistent during
this period and patients may be tenuous due to severe hypoxemia.
• Most patients who survive this initial course begin to exhibit better
oxygenation and decreasing alveolar infiltrates over the next several days.
• Some patients, however, have persistent, severe hypoxemia and remain
ventilator-dependent. Pulmonary proliferative changes and fibrosis may
progressively replace the pathological findings of diffuse alveolar damage
as early as ten days after the onset of the respiratory failure.
• The fibroproliferative phase of ARDS is characterized radiographically by
progression from airspace opacification to a more coarsely reticular
pattern of lung infiltration. These changes within the lung parenchyma are
often accompanied by persistent hypoxemia, low lung compliance, high
dead space, and sometimes by progressive pulmonary hypertension. The
course may become dominated by persistent ventilator dependence and
various complications.
Complications
Patients with ARDS are at high risk for
complications.
• Some complications are related to mechanical
ventilation
pulmonary barotrauma,
nosocomial pneumonia,
• while others are related to critical illness and
being in the intensive care unit
delirium,
deep venous thrombosis,
gastrointestinal bleeding due to stress ulceration,
catheter-related infections.
Other complications
• Other complications that frequently occur
during the hospital course of patients with
ARDS include the following:
• Deep venous thrombosis
• Gastrointestinal bleeding due to stress
ulceration
• Poor nutrition
• Catheter-related infections
DIAGNOSTIC EVALUATION
Excluding cardiogenic pulmonary edema
• An absence of cardiac exam abnormalities (eg, an S3 or
S4 gallop, new or changed murmur),
• elevated right-sided filling pressures (eg, elevated
jugular venous pressure),
• certain radiographic abnormalities (eg, pulmonary
venous congestion, Kerley B lines, cardiomegaly, and
pleural effusions),
helps distinguish ARDS from cardiogenic pulmonary
edema.
Several additional diagnostic tests may also be helpful,
including measurement of plasma brain natriuretic
peptide levels, echocardiography, and right heart
catheterization:
Brain natriuretic peptide (BNP)
• A plasma BNP level below 100 pg/mL favors
ARDS, but higher levels neither confirm heart
failure nor exclude ARDS . This derives from an
observational study of patients with ARDS (n =
33) or cardiogenic pulmonary edema (n = 21) .
The study found that a plasma BNP level less than
100 pg/mL identified ARDS with a sensitivity,
specificity, positive predictive value, and negative
predictive value of 27, 95, 90, and 44 percent,
respectively.
Echocardiography
• Many clinicians use transthoracic echocardiography as
the first-line diagnostic test if cardiogenic pulmonary
edema cannot be excluded by clinical evaluation and
measurement of the BNP level. While severe aortic or
mitral valve dysfunction, severe diastolic dysfunction,
or a severely reduced left ventricular ejection fraction
favors cardiogenic pulmonary edema, the latter is
insufficient to confirm primary cardiogenic pulmonary
edema because some precipitants of ARDS (eg, septic
shock) can cause an acute, severe cardiomyopathy that
develops concomitantly with ARDS.
Right heart catheterization
• There is evidence that there is generally no
value to routine right heart catheterization for
either the diagnosis or management of ARDS .
However, pulmonary artery catheterization
may be considered if primary cardiogenic
pulmonary edema cannot be excluded on the
basis of the clinical evaluation, plasma BNP
measurement, and echocardiogram.
Excluding other causes of hypoxemic
respiratory failure
• Noninvasive respiratory sampling – The lower
respiratory tract can be sampled via
tracheobronchial aspiration or minibronchoalveolar lavage (mini-BAL).
• Regardless of the technique, the specimen that is
obtained may be evaluated via microscopic
analysis (eg, Gram stain, cytology) and
microbiologic culture; these studies may identify
pneumonia or rapidly progressive cancer as the
correct diagnosis
• Flexible bronchoscopy – Flexible
bronchoscopy can obtain lower respiratory
samples for microscopic analysis and
microbiologic culture if the noninvasive
techniques are unsuccessful. It can also
identify abnormalities that may not be
detected with noninvasive sampling.
Therefore, flexible bronchoscopy is a
reasonable next step whenever noninvasive
sampling is nondiagnostic.
• Lung biopsy – Surgical lung biopsy may be considered when
alternative causes of acute hypoxemic respiratory failure cannot be
excluded on the basis of the clinical context, symptoms, signs, and
bronchoscopy . The safety of lung biopsy in selected patients with
hypoxemic respiratory failure was demonstrated by a retrospective
study of 57 patients with ARDS who underwent open lung biopsy .
The patients had a mean ratio of arterial oxygen tension to fraction
of inspired oxygen (PaO2/FiO2) of 145 mmHg and the rate of major
complications was 7 percent, with no deaths attributed to the
biopsy. Although the complication rate was 39 percent, most were
tolerable (eg, persistent air leaks).
• The results of the biopsy resulted in the addition of specific therapy
in 60 percent of patients and the withdrawal of unnecessary
therapy in 37 percent.
DIAGNOSTIC CRITERIA
• Berlin definition — ARDS can be diagnosed
once cardiogenic pulmonary edema and
alternative causes of acute hypoxemic
respiratory failure and bilateral infiltrates have
been excluded. The Berlin Definition of ARDS
requires that all of the following criteria be
present to diagnose ARDS
DIAGNOSTIC CRITERIA
• Respiratory symptoms must have begun within one
week of a known clinical insult, or the patient must
have new or worsening symptoms during the past
week.
• ●Bilateral opacities consistent with pulmonary edema
must be present on a chest radiograph or computed
tomographic (CT) scan. These opacities must not be
fully explained by pleural effusions, lobar collapse, lung
collapse, or pulmonary nodules.
• ●The patient’s respiratory failure must not be fully
explained by cardiac failure or fluid overload. An
objective assessment (eg, echocardiography) to
exclude hydrostatic pulmonary edema is required if no
risk factors for ARDS are present.
• ●A moderate to severe impairment of oxygenation must be
present, as defined by the ratio of arterial oxygen tension
to fraction of inspired oxygen (PaO2/FiO2). The severity of
the hypoxemia defines the severity of the ARDS:
• •Mild ARDS – The PaO2/FiO2 is >200 mmHg, but ≤300
mmHg, on ventilator settings that include positive endexpiratory pressure (PEEP) or continuous positive airway
pressure (CPAP) ≥5 cm H2O.
• •Moderate ARDS – The PaO2/FiO2 is >100 mmHg, but ≤200
mmHg, on ventilator settings that include PEEP ≥5 cm H2O.
• •Severe ARDS – The PaO2/FiO2 is ≤100 mmHg on ventilators
setting that include PEEP ≥5 cm H2O.
DIFFERENTIAL DIAGNOSIS
• A variety of alternative conditions may
present as acute hypoxemic respiratory failure
with bilateral alveolar infiltrates and,
therefore, should be considered whenever
ARDS is suspected
Cardiogenic pulmonary edema
• Cardiogenic pulmonary edema is usually due to left
ventricular systolic or diastolic dysfunction, but may also be
due to fluid overload, severe hypertension, renal artery
stenosis, or severe renal disease. Its presentation is nearly
identical to ARDS, except there may be evidence of cardiac
dysfunction (eg, an S3 or S4 gallop, new or changed
murmur), elevated right-sided filling pressures (eg, elevated
jugular venous pressure), or related radiographic
abnormalities (eg, pulmonary venous congestion, Kerley B
lines, cardiomegaly, and pleural effusions). Distinguishing
cardiogenic pulmonary edema from ARDS can be aided by
measurement of a brain natriuretic peptide (BNP) level,
echocardiography, and, less often, right heart
catheterization
An acute exacerbation of idiopathic
pulmonary fibrosis
• An acute exacerbation of idiopathic pulmonary fibrosis
or other chronic interstitial lung diseases can closely
resemble ARDS in both clinical presentation and chest
radiographic abnormalities. Like ARDS, the pathological
findings are dominated by diffuse alveolar damage, but
the prognosis is substantially worse. This diagnostic
possibility is easily overlooked in patients whose
underlying interstitial lung disease is unknown or mild
or moderate in severity. The diagnosis is suggested by
careful review of previous chest radiographic images,
by discovery of subpleural reticular changes intermixed
with alveolar opacities on a chest CT scan obtained
shortly after onset of ARDS, or by surgical lung biopsy.
Diffuse alveolar hemorrhage
• Diffuse alveolar hemorrhage may be associated
with a large, otherwise unexplained drop in the
hemoglobin concentration and hematocrit. While
hemoptysis may be minimal or absent,
bronchoscopy often reveals frothy bloody
secretions throughout the airways and invariably
detects an increasing amount of red blood cells in
serial bronchoalveolar lavage specimens.
• The recovery of hemosiderin-laden macrophages
from bronchoalveolar lavage fluid is strongly
suggestive of diffuse alveolar hemorrhage.
Idiopathic acute eosinophilic
pneumonia
• Idiopathic acute eosinophilic pneumonia
(IAEP) occurs in previously healthy individuals
and is characterized by cough, fever, dyspnea,
and sometimes chest pain.
• Bronchoalveolar lavage specimens always
contain a large number of eosinophils,
typically 35 to 55 percent of all recovered cells
• Peripheral eosinophilia may or may not be
present [
Cryptogenic organizing pneumonia
• Cryptogenic organizing pneumonia (COP) often mimics
community-acquired pneumonia with an onset that is
heralded by a flu-like illness with fever, malaise, fatigue,
and cough. The most common features at presentation are
a persistent nonproductive cough, dyspnea with exertion,
and weight loss. Bronchoalveolar lavage usually contains a
smaller proportion of macrophages and higher proportions
of lymphocytes, neutrophils, and eosinophils than healthy
patients. This "mixed pattern" of increased cellularity is
thought to be characteristic of COP. The diagnosis is made
by ruling out infectious causes of pneumonia and
documenting typical pathologic changes in tissue obtained
by open lung biopsy
Acute interstitial pneumonia
• Acute interstitial pneumonia (Hamman-Rich
syndrome) is a rare and fulminant form of diffuse
lung injury that has a presentation similar to
ARDS. Many people consider acute interstitial
pneumonia a subset of idiopathic ARDS since its
clinical manifestations are similar and both
demonstrate diffuse alveolar damage on
histopathology. The distinguishing characteristic
is that ARDS is often associated with a known risk
factor, whereas acute interstitial pneumonia is
not.
Cancer
• Cancer can disseminate through the lungs so
rapidly that the ensuing respiratory failure
may be mistaken for ARDS. This is most often
due to lymphoma or acute leukemia, but
lymphangitic spread of solid tumors
occasionally behaves this way. Cytological
preparation of bronchoscopic specimens (eg,
brushings, lavage) may reveal malignant cells.
MANAGEMENT OF HYPOXEMIA
— By definition, patients with ARDS are severely hypoxemic. Options available
for improving arterial oxygen saturation (SaO2) include:
●Use of high fractions of inspired oxygen (FiO2)
●Decrease oxygen consumption
●Improve oxygen delivery
●Manipulate mechanical ventilatory support
Treatment
Medications
• Medications directed at the underlying cause of ARDS are
indicated
• Intravascular volume should be maintained at the lowest
level required to maintain adequate cardiac output
• Diuretics may be needed to reduce pulmonary capillary
wedge pressure and improve oxygenation
• Cardiac output that falls when PEEP is used may be
improved by reducing the level of PEEP or by the judicious use
of inotropic drugs (eg, norepinephrine)
• Achieving supranormal oxygen delivery through the use of
inotropes and blood transfusion is not clinically useful and
may be harmful
• Sedatives, analgesics, and antipyretics may be used to
decrease oxygen consumption
• Systemic corticosteroids have not been shown to reliably
improve outcomes
Therapeutic Procedures
• Intubation and mechanical ventilation are
usually required to treat hypoxemia
• Use the lowest levels of PEEP and Fio2 needed
to maintain Pao2 > 55 mm Hg (7.13 kPa) or the
Sao2 above 88%
• Mechanical ventilation with small tidal
volumes (6 mL/kg of ideal body weight) has
been shown to reduce mortality by 10% in a
multicenter trial
•• Prone positioning may improve oxygenation
in selected patients
Supine Ventilation
• ± 40% lung volume under heart, especially patients
with large hearts
Prone Ventilation