Introduction
The bedside chest radiograph is an indispensable diagnostic tool in the management
of critical patients admitted in the intensive care unit (ICU). Studies have shown
that up to 65% of ICU chest films may reveal a significant or unsuspected process.
The American College of Radiology (ACR) suggests that daily chest radiographs be obtained
on patients with acute cardiopulmonary problems and those receiving mechanical ventilation.[[1]] The present manuscript attempts to integrate clinical and radiographic perspectives
of typical ICU syndromes and conditions seen in ICUs around the world.
Acute respiratory distress syndrome (ARDS)
ARDS is a rapidly progressive hypoxemic state due to diffuse alveolar damage resulting
in permeability edema which is independent of concurrent cardiac disease[[1],[2],[3],[4],[5]] and has a high fatality rate of 50%.[[3]] It can result from direct injury to lung (pneumonia, aspiration, near drowning,
or inhalational injury) or secondary to systemic pathologies, such as pancreatitis,
severe trauma, extensive burns, and drug overdose.[[3]]
The findings on a chest radiograph are stereotypical and evolve as three overlapping
phases.[[4]] Following an insult, there is a short period of radiographic latency. The earliest
findings include those of an interstitial pattern, shortly followed by alveolar flooding
of protein rich fluid resulting in air space opacification [[Figure 1A]]. Thus, Kerley B lines may be seldom radiographed.[[4]] The alveolar edema then progresses rapidly within the next 48–72 h passing from
patchy opacities to diffuse consolidation[[3],[4],[5]] [[Figure 1B]]. The fact that this appearance cannot be fully explained by presence of pleural
effusion, atelectasis, or pulmonary nodules[[2]] is a clue to diagnosis. The plain film features of exudative phase often mimic
that of cardiogenic pulmonary edema; however, absence of cardiomegaly, normal vascular
pedicle and lack of apical vascular redistribution, peribronchovascular cuffing and
pleural effusion in the former help arrive at a diagnosis [[Figure 2]]. Further, a near constant radiographic appearance demonstrated by daily portable
x-ray favors ARDS over pulmonary edema[[4]] which quickly clears on improving the hemodynamic alterations.[[3],[4],[5]] However, there exists a host of confounding factors like coexistence of ARDS and
cardiogenic pulmonary edema especially when ARDS complicates a case of sepsis, presence
of pleural effusion in ARDS, and heart failure in a normal sized heart.[[3]] Pulmonary contusion may also share a few imaging features with ARDS[[3]] [[Figure 3]]. However, the former is characterized by localized opacities which are both earlier
to appear as well as undergo faster resolution than ARDS.
Figure 1 (A and B): (A) Early “exudative phase”-Development of patchy air space consolidations bilaterally
(black arrows) resembling alveolar edema. (B) “Proliferative phase”–Visible increase
in air space opacities forming coalescent consolidations (black arrow), predominantly
in lower zones (asterisk). Note the classic presence of air bronchograms (white arrow)
Figure 2: Diffuse, bilateral reticular opacities (black arrows), presence of air bronchograms
(black arrowhead), normal vascular pedicle width (white arrows), no “cephalization”
of vasculature, normal cardiothoracic ratio, and absent pleural effusions– these findings
help zero in on the diagnosis of ARDS
Figure 3: Multifocal patchy air space opacities (black arrows) - pulmonary hemorrhage, a mimicker
of ARDS
Progression to proliferative stage is marked by appearance of ground glass opacities.
The radiographic appearances of this phase usually stabilize and remain static for
a variable period. Hence, the appearance of new air space opacities would mean superadded
infections or ARDS related complications[[4]] [[Figure 4]]. Finally, there may be resolution of x- ray findings[[3],[4],[5]] or persistence of coarse reticular pattern (in 10% of survivors) or formation of
subpleural and or intraparenchymal cysts which when rupture result in pneumothorax.[[3],[4],[5]]
Figure 4: Patient under treatment for ARDS with focal patchy consolidation in right mid and
lower zone (asterisk)-frequently seen complication of superimposed pneumonia. Intubation
may induce complications of barotrauma - pneumothorax in left hemithorax (white arrows)
with medial collapse of left lung (black arrow). Chest drain in situ with associated
subcutaneous emphysema (curved black arrow)
Patients with ARDS frequently need positive-end expiratory pressure ventilation (contrary
to pulmonary edema). A chest radiograph may help tailor the ventilator settings in
this regard. Further, serial x-rays may depict changes of barotrauma namely interstitial,
mediastinal, subcutaneous emphysema, and pneumothorax[[4]] [[Figure 4]].
Pulmonary edema
Pulmonary edema can be a cause of admission in an ICU or conversely occur during the
course of ICU stay.[[5]] This transmigration of fluid may be a result of an imbalance between hydrostatic
and oncotic pressures, changes in capillary permeability, or a combination of both.[[6]] The former is generally seen secondary to cardiac failure, overhydration, or renal
insufficiency.[[1]]
The increased hydrostatic pressure edema has two phases.[[1],[6]] An increase of 15 to 25 mm Hg in transmural arterial pressure marks the beginning
of interstitial edema. Classic findings in this stage include blurring of vascular
markings, appearance of Kerley B lines, subpleural effusions, and peribronchial cuffing[[1],[5],[6]] [[Figure 5A], [B], [C]]. With continued increase in transmural arterial pressure, typically in excess of
25 mm Hg, alveolar flooding is evident which is characterized by appearance of tiny
nodular or acinar shadows.[[6]] Further worsening may result in frank consolidation. The classic bat-wing edema
is seen in 10% of patients and displays a perihilar distribution owing to rapidly
progressive alveolar flooding[[6]] [[Figure 5D]].
Figure 5 (A-D): (A) Earliest changes of pulmonary edema (CVP 10-25 mmHg): redistribution of pulmonary
veins- “cephalization” (curved white arrows). (B) With increasing pressure (CVP 20–25
mmHg), transudation of fluid around bronchi seen as peribronchial cuffing (curved
black arrows). (C) Interstitial edema within lymphatics - Kerley B lines [thin, short
lines 1–2 cm in length, at the periphery perpendicular to pleural surface] (black
arrows). Other features seen are cardiomegaly, indistinctness of pulmonary vessels
(asterisks), and early changes of perihilar bat wing opacities (white arrows). (D)
At CVP 25- 30 mm Hg, fluid accumulates in alveoli producing classic perihilar batwing
or angel wing consolidation (black arrow heads). Increased vascular pedicle width
(black arrows) points to a likely underlying renal pathology (overhydration), leading
to pulmonary edema
Variability in appearances of pulmonary edema may be due to lung parenchymal changes
(Chronic Obstructive Pulmonary Disease, fibrosis due to tuberculosis), specific conditions
(right upper lobe involvement in acute mitral regurgitation), and patient position.
These may result in a unilateral, lobar, or lower zone distribution or a miliary pattern[[1],[6]] [[Figure 6]].
Figure 6: Cardiomegaly with cephalization of pulmonary vessels (black arrow) and patchy right-sided
air space opacities (white arrows) - Right-sided unilateral pulmonary edema. Unilaterality
can be mistaken for pneumonia, pulmonary hemorrhage, aspiration
The permeability edema of ARDS can be distinguished from hydrostatic pressure edema
based on the presence of cardiomegaly and a vascular pedicle more than 7–8 cm in the
latter[[5]] [[Figure 7]].
Figure 7: Measurement of vascular pedicle width: Draw a perpendicular A at the junction of
left subclavian artery with aorta. Draw a perpendicular B at the intersection of superior
vena cava with right mainstem bronchus. Normal width: 7–8 cm
Ventilator-associated pneumonia
Ventilator-associated pneumonia (VAP) is a polymicrobial pneumonia that occurs 48–72
h after intubation.[[7]] It constitutes 50% of cases of hospital acquired pneumonia and occurs in 9–27%
of mechanically ventilated patients.[[7]] It is the leading cause of death in ICU patients[[1]] and hence its early diagnosis is crucial. However, both clinical as well as radiographic
criteria to diagnose the condition are nonspecific.[[1],[5],[7],[8]]
Typical plain film findings in VAP include patchy areas of consolidation or poorly
defined opacities which are often multifocal[[1],[5]] [[Figure 8]]. Additional finding of pleural effusion favors this diagnosis. Absence of volume
loss makes atelectasis an unlikely consideration. Likewise, a change in pattern over
hours (following correction of hemodynamics) is a tell-tale sign of pulmonary edema.[[5]] About a third of patients may be missed based on clinical evaluation.[[7]] Hence, complications like abscess [[Figure 9]], pleural empyema, and bronchopleural fistula may be more commonly encountered in
them.[[1]] It is of prime importance to bear in mind that a negative chest x-ray does not
exclude the possibility of VAP, particularly in immunocompromised patients.[[5]]
Figure 8: Patchy areas of multifocal opacities in right lung fields (asterisk) – developing
ventilator associated pneumonia
Figure 9: Multiple round opacities demonstrating air fluid levels in right lung fields (curved
black arrows) - abscess formation as a complication of pneumonia
Atelectasis
Atelectasis is defined as failure of the lung or part of it to expand completely.[[1]] It may be caused by an endobronchial obstructive pathology or alternatively by
pleural fluid, pneumonia or lymph nodes compressing the bronchus, resulting in compressive
atelectasis.[[5]] Statistically, atelectasis is the leading cause of radio-opacity on a chest film
in an ICU setup.[[5]]
Roentgenographic findings include an increase in opacity and signs of volume loss
namely displacement of fissures and hilum, crowding of pulmonary vessels, hilum, deviation
of trachea, unilateral elevation of diaphragm, and compensatory overinflation[[1],[5]] [[Figures 10] and [11]]. However, the signs may often be subtle leading to a misdiagnosis.
Figure 10: Homogenous air space opacity in right upper zone (arrow head) with absent air bronchogram,
upward fissural displacement (black arrows), tracheal pull (interrupted black arrow)
Figure 11: Left-sided atelectasis with crowding of ribs (bracket), ipsilateral mediastinal shift
(interrupted arrows), elevation of hemidiaphragm (arrowheads)
A lower lobe collapse presents with a wedge shaped radio-opacity that points toward
the hilum and obscures the respective hemidiaphragm with downward, posterior, and
medial migration of the atelectatic lobe.[[1],[9]] An underpenetrated film may miss the retrocardiac atelectatic lobe in case of marked
collapse of left lower lobe.[[9]] Atelectasis of right middle lobe or lingula on left presents with subtle increase
in density with loss of discreteness of cardiac borders.[[9]] A lateral film shows the collapse to a better advantage.
With collapse of right upper lobe, the lesser fissure migrates superiorly and medially
resulting in a triangular radiopacity[[9]] [[Figure 10]]. On the contrary, the left upper lobe collapses anteriorly and upward with a faint
lateral margin (because of absence of minor fissure on the left).[[1],[9]] The loss of interface with the aortic knob that occurs with collapse may sometimes
be occupied by radiolucency of hyperexpanded left lower lobe (luftsichel sign).
Pulmonary thromboembolism
Acute pulmonary thromboembolism (APTE) is frequently unsuspected and underdiagnosed.[[1]] Although radiographic findings of APTE are subtle and usually nonspecific; the
key role of a plain film is to exclude alternate diagnoses.[[1]] Cardiomegaly is the most common finding.[[10]] The enlargement of right heart and the azygous system of veins is secondary to
acute pulmonary hypertension.[[11]]
Atelectasis is yet another common finding in APTE and presents as subsegmental curved
lines that abut the pleural surface.[[11]] Pleural effusion howsoever nonspecific is reported to be present in 50% of cases
of APTE. The effusion is serous, generally bilateral, and mild in quantity.[[1],[11]] Occurrence of specific signs like enlargement of right descending pulmonary artery
(Palla’s sign)[[1],[11],[12]] or the central one (Fleischner’s sign),[[12]] abrupt tapering of pulmonary artery (knuckle sign),[[12]] oligemia beyond the site of occlusion (Westermark sign)[[1],[11],[12]] [[Figure 12A] and [B]], and a triangular radiopacity that lacks air bronchogram with the apex pointing
toward hilum (Hampton’s hump) [[Figure 13]] is uncommon.[[11]] Similarly, pulmonary infarction is rare and usually manifests as multifocal consolidation,
12–24 h following an embolic event with a propensity to involve the basal segments.[[1]]
Figure 12 (A and B): Bilateral lucent areas (white circles) representing oligemia in a patient (A) with
computed tomography (B) suggestive of bilateral pulmonary emboli (white interrupted
arrows)
Figure 13: A pleural-based triangular opacity (inset) seen in left lower lobe representing “Hampton’s
hump”- an area of peripheral infarction secondary to pulmonary embolism with blunting
of right costophrenic angle (asterisk) representing pleural effusion
Aspiration
Aspiration of gastric and/or oropharyngeal secretions is common in mental obtundation,[[13]] placement of endotracheal or nasogastric tubes[[1]] or tracheostomy with manifestations varying from mild bronchiolitis to hemorrhagic
pulmonary edema. The condition further worsens owing to secondary infection or may
resolve without any complications.
Chest x-ray features in aspiration are nonspecific[[13]] with variability being the hallmark. Common appearances include small irregular
shadows present singly or in combination with confluent or acinar infiltration.[[13]] The distribution of these opacities depends on patient position, gravity, and dynamics
of air flow with perihilar and basal[[1],[13]] or superior segment of lower lobe [[Figure 14]] and posterior segment of upper lobe[[14]] being the commonest. The diagnosis of aspiration needs to be entertained in the
correct clinical setting with rapidly and extensively developing pulmonary infiltrates
in a previously normal documented radiograph, an uncomplicated course with prompt
resolution, normal cardiac silhouette, and absence of pleural effusion.[[13]]
Figure 14: Patchy air space opacity with absent air bronchogram in left lower zone (asterisk)
with reticular opacities in right lower zone (black arrows)- dependent opacities in
aspiration
Neurogenic Pulmonary Edema
Neurogenic pulmonary edema (NPE) is seen in patients with subarachnoid hemorrhage,
status epilepticus, and trauma.[[6],[15]] It is a rare event. A massive adrenergic drive following the severe neural insult[[15]] triggers a mixed pulmonary edema (hydrostatic pressure and permeability edema)
without diffuse alveolar damage.
NPE may develop within seconds to minutes after a seizure activity and resolves in
24–48 h.[[6]] Chest radiographic findings are those of cardiogenic pulmonary edema [[Figure 15]] and hence diagnosis of NPE is one of exclusion. It is important to recognize NPE
as hypoxemia caused by the pulmonary event may further aggravate the initial neural
insult.[[15]]
Figure 15: Frontal radiograph of a patient with stroke taken 6 h post thrombolysis shows bilateral,
homogenous, upper zone predominant alveolar opacities (arrow heads), and bilateral
blunting of costophrenic angles (black arrows) suggesting pleural effusion. Repeat
radiograph after 3 days was normal- neurogenic pulmonary edema
A comparison of the various entities has been provided below [[Table 1]].
Table 1
Comparison of radiographic findings in each pathology
|
Radio graphic finding
|
ARDS
|
Pulmonary edema
|
Ventilator-associated pneumonia
|
Atelectasis
|
APTE
|
Aspiration
|
Neurogenic pulmonary edema
|
|
Vascular pedicle width
|
Normal
|
Widened
|
Normal
|
Normal
|
Normal
|
Normal
|
Normal
|
|
Cardiac size
|
Normal
|
Increased
|
Normal
|
Normal
|
Increased
|
Normal
|
Increased
|
|
Hilar prominence
|
Absent
|
Present
|
+/-
|
Absent
|
Present
|
Absent
|
Present
|
|
Pleural effusion
|
Absent
|
Present
|
Present
|
+/-
|
+/-
|
Absent
|
Present
|
|
Pulmonary opacities
|
Patchy, diffuse
|
Perihilar
|
Focal/Multifocal
|
Lobar specificity
|
Subpleural, basal
|
Dependent
|
Perihilar, upper zone
|
|
Interstitial markings
|
Present
|
Present
|
Absent
|
Absent
|
Absent
|
Present
|
Present
|
|
Volume loss
|
Chronic change
|
Absent
|
Absent
|
Present
|
+/-
|
Absent
|
Absent
|
|
Silhouette sign
|
+/-
|
+/-
|
Present
|
Present
|
+/-
|
+/-
|
+/-
|
|
Resolution
|
Delayed/fibrosis
|
Early
|
Delayed, complications +/-
|
Variable
|
Delayed/absent
|
Early
|
Early
|
In order to ensure accuracy, radiologists can refer to a checklist prior to preparing
a report as follows:
-
Is there cardiomegaly?
-
Is there any abnormality of vascular markings- hilar prominence/cephalization of vessels/prominent
descending pulmonary arteries?
-
Are there interstitial markings, Kerley lines seen?
-
Pulmonary opacities
-
distinguishable from overlying lines and tubes?
-
persistent or newly developed?
-
with air bronchogram?
-
do they conform to any specific underlying pathology?
-
with features of volume loss?
-
is there any loss of silhouette?
-
secondary cavitation?
-
progression on serial radiographs?
-
Costophrenic angles, major and minor fissures to be evaluated for pleural effusion
-
Lines and tubes
-
type of device
-
appropriate positioning
-
secondary complications
-
barotrauma
-
Bony cage
-
fractures or dislocation of ribs (or flail chest)/vertebrae sternum/clavicle/scapula
-
deformities of bony cage
-
post-procedural changes: sternotomy wires vertebroplasty/kyphoplasty/spinal fixation/thoracotomy
and associated complications
-
Soft tissue structures - subcutaneous emphysema/soft tissue lesion/postoperative changes
(e.g., mastectomy)
-
Abdomen- pneumoperitoneum/pathological calcifications/bowel gas pattern
-
Comparison of serial radiographs.
