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3
The Role of Chest Radiography in the Critical Care Unit
67
3.2 Lines andTubes [5, 6]
The evaluation of equipment is critical when imaging patients in ICUs. Early detection of malpositioning minimizes the risk of complications.
3.2.1 Endotracheal andTracheostomy Tubes
Endotracheal tubes (Fig. 3.2) are used to provide mechanical ventilation to the
patients who require short-term respiratory support. The tip of the tube must be
positioned 4–6cm above the carina. However, neck exion may cause the tube to
descend by up to 2cm, while neck extension may cause it to ascend by up to 2cm.
An improperly positioned endotracheal tube can cause subsegmental atelectasis,
lung collapse, pneumothorax, unintended extubation, larynx damage, esophageal
intubation, and aspiration. Right-sided important bronchus intubation is more common due to the top angle of the right bronchus. Tracheostomy tubes are used for
long-term intubation. The tube must be placed at the T3 stage and maintained with
neck exion and extension. The tube diameter must be 2/3 of the trachea’s length,
and the cuff ought not to distend the tracheal wall. Mediastinal air may be visible
after tube placement.
Fig. 3.2 Endotracheal
tube (arrow), central
venous catheter
(arrowhead), and
nasogastric tube (curved
arrow)
68
F. Macori
ab
Fig. 3.3 Malposition of the nasogastric tube, inserted in the right bronchus, more frequent due to
the angle of its origin (a), and left bronchus (b)
3.2.2 Nasogastric Tube
Gastroenteric tubes are used for feeding, drug administration, and suctioning. The
best position of the tube tip is in the gastric antrum or the duodenum because it
reduces the risk of aspiration (Fig.3.2). Radiography is vital in detecting any odd
vicinity of the tube, which could otherwise cause life-threatening headaches. Rare
complications encompass pharyngeal and esophageal perforations. Tubes coiling
within the pharynx or esophagus can create a high chance of aspiration. Enteric
tubes terminating inside the trachea or bronchi (Fig.3.3a, b) can cause bronchopulmonary damage and pneumonia. If the lung parenchyma is punctured, pneumothorax, pulmonary laceration, and pulmonary contusion should be considered.
Therefore, an observe-up radiograph is vital if an enteric tube is placed within
the airway.
3.2.2.1
Chest
Tubes
Tube thoracostomy is often used for the removal of uid or air from the pleural
space (Fig.3.4). The appropriate placement of a chest tube relies on whether the
purpose is to remove air or uid from the pleural space. For a pneumothorax evacuation, the tube’s tip should face upwards, while it should face downwards for uid
drainage. In the case of loculated pleural uid, the chest tube should be placed in the
exact location of the loculation for effective drainage.
Improper placement of a chest tube can lead to ineffective pleural drainage. A
radiopaque stripe on a radiograph can identify the tip and holes. The side hole
should always be medial to the ribs’ inner margin. Poor visualization of the nonopaque wall of the tube can indicate inadvertent placement in extrapleural soft
tissues.
The Role of Chest Radiography in the Critical Care Unit
3
Fig. 3.4 Chest tube
(arrow) of the right thorax.
The study shows the
ndings of a bilateral
pneumonia with pleural
effusion and the history of
sternotomy. The
nasogastric tube is under
the diaphragm, in the left
quadrant
69
Ineffective drainage with chest tubes may be due to tube kinking, clotted blood
or debris blockage, or tube tip blockage by the mediastinum. Chest tube advancement into the mediastinum can rarely cause heart or great vessel injury. Inserting the
chest tube through the diaphragm into the abdomen may result in damage to the
liver, spleen, and stomach.
After prolonged pulmonary atelectasis, re-expansion pulmonary edema occurs
when air or uid is rapidly removed from the pleural space. Symptoms can appear
2–48h after lung re-expansion and may last up to 2days. Radiographic ndings
include unilateral airspace opacity, and CT scans may show ground-glass opacities,
consolidation, and septal thickening. The exact cause is not fully known, but it is
believed to be linked to increased pulmonary vascular permeability and depletion of
surfactant.
A residual pleural or parenchymal line may appear on a chest radiograph after
removing a chest tube, outlining the previous tube tract. It is important not to mistake this line for a pneumothorax.
3.2.3 Central Venous Catheters
Central venous catheters (CVCs) are used for venous access and central venous
pressure monitoring in critically ill patients (Fig.3.2). They can be placed through
the subclavian, internal jugular, or femoral veins. Smaller catheters can be inserted
through antecubital veins and remain for months. The CVC tip should be in the
superior vena cava, just below the rst rib, and slightly above the right atrium. The
right atrium should be avoided to prevent arrhythmia, myocardial rupture, and cardiac tamponade.
70
ab
F. Macori
It is important to verify the correct positioning of a central venous catheter
(CVC) through radiography, as malpositioning can occur in up to 40% of cases.
Misplacement can affect central venous pressure measurement accuracy and cause
adverse effects due to the infusion of potentially toxic substances. Misplaced CVCs
can terminate in the right heart or central systemic veins. Inadvertent catheterization
of the subclavian artery will present with a pulsatile ow in the catheter and an
abnormal catheter position on a radiograph.
Pneumothorax is a common complication after CVC insertion, occurring in up to
5% of cases. Always get a chest radiograph after CVC placement. In the ICU, an
upright or contralateral decubitus radiograph detects small pneumothoraxes, which
can become larger in positively ventilated patients.
Vascular perforation during catheterization is life-threatening. Radiographic
ndings indicating vascular injury include unusual catheter placement, apical cap,
new pleural effusion, and mediastinal widening. The catheter’s gently curved tip
and its position against the lateral wall of the SVC may indicate a venous perforation. Extravascular positioning can cause uid buildup in the mediastinum or pleural space. A contrast medium can conrm proper catheter placement.
The catheter may knot, loop, or kink during placement. Prolonged placement can
cause venous thrombosis, leading to pulmonary embolism. In 1% of cases, the catheter may fragment, causing “pinch-off syndrome.” Fragmentation can result in
arrhythmia, pulmonary embolism, or death. Minimally invasive endovascular
retrieval techniques can recover catheter fragments.
Fig. 3.5 Dual-lead pacemaker correctly positioned (a) and with a displaced lead (b) (arrow)
3 The Role of Chest Radiography in the Critical Care Unit
71
3.2.4 Cardiac Devices
Temporary and permanent cardiac pacemakers are used to treat conduction abnormalities (Fig.3.5). Transvenous pacing is the preferred method for temporary pacing in the ICU; permanent pacemakers consist of a pulse generator implanted in the
chest wall and lead wires with electrodes. They range from single lead to complex
devices. Biventricular pacing or cardiac resynchronization therapy is a treatment
option for severe congestive heart failure. The left ventricular pacing electrode can
be inserted through the coronary sinus to stimulate the left ventricular myocardium.
Combining an automatic implantable cardioverter-debrillator (AICD) with a pacemaker can provide an additional benet for these patients. AICD devices may have
a single high-voltage shock coil or an additional coil in the SVC or brachiocephalic
vein. External pacemaker-debrillators are also commonly used in the ICU.
Electrode insertion can cause pneumothorax, vascular injury, and myocardial
perforation (usually in the right ventricle). When the electrode tip extends beyond
the heart’s border, it is important to recognize and monitor for pericardial effusion
and cardiac tamponade.
Lead fractures in pacemakers occur for various reasons, such as compression of
the lead between the clavicle and the rst rib or manipulation of the implanted pulse
generator by the patient. Technological advancements have decreased the incidence
of such fractures to 1–4%.
3.2.5 Arterial Catheters
The Swan-Ganz catheter measures pulmonary capillary wedge pressure to differentiate between cardiogenic and noncardiogenic pulmonary edema in critically ill
patients.
A catheter is inserted into the main pulmonary arteries through the subclavian or
internal jugular vein. The catheter tip should not extend beyond 2cm of the hilum.
Inating the balloon should only happen during measurements. Pulmonary infarction
can occur if the catheter is too distal, if the balloon is persistently inated, or if a clot
forms. A chest radiograph can determine the infarction as a wedge-shaped opacity.
CVC insertion complications such as misplacement, looping, coiling, knotting,
pneumothorax, and vascular injury may occur in pulmonary artery catheter placement. Rare but serious complications include pulmonary artery rupture, dissection,
and pseudoaneurysm. Pseudoaneurysm may cause new pulmonary nodules months
after catheter removal. Balloon rupture and pulmonary artery-bronchial tree stula
are other rare complications.
72
Fig. 3.6 Bilateral
perihilar, mid, and lower
zone predominant
consolidation, most
consistent with pulmonary
edema. Moderate bilateral
pleural effusions
Fig. 3.7 Right perihilar,
mid, and lower zone
predominant consolidation
in keeping with pulmonary
edema
F. Macori
3.3 Cardiopulmonary Abnormalities
Several potential causes of increased lung opacication exist, but only a few are commonly seen in the ICU setting. These include pulmonary edema, pneumonia, atelectasis, and aspiration. The imaging characteristics of these entities are outlined below.
3 The Role of Chest Radiography in the Critical Care Unit
73
3.3.1 Pulmonary Edema
Pulmonary edema [7] is a frequent cause of diffuse parenchymal opacication in
ICU patients (Figs.3.6 and 3.7). It is important to differentiate between hydrostatic
pulmonary edema (cardiogenic edema) and increased capillary permeability edema
(noncardiogenic edema). While certain features can help distinguish between the
two, it is only sometimes possible to differentiate them based solely on radiographic ndings. Additionally, a patient may have both types of edema
simultaneously.
Hydrostatic pulmonary edema, which is typically caused by congestive heart
failure or volume overload, follows a predictable course. Increased pulmonary vascularity is followed by the sequential development of uid in the interstitial compartments of the lungs and, subsequently, in the airspaces.
The interstitial compartment of the lungs has two major components: the peribronchovascular sheath and the interlobular septa. Fluid in the peribronchovascular
sheath results in indistinct pulmonary vessels (“hilar haze”) (Fig.3.9) and peribronchial cufng. This occurs when pulmonary venous pressures exceed the normal
range of 8–12mmHg. Fluid in the interlobular septa creates Kerley B (Fig.3.10) or
septal lines, which are linear opacities visible in the lung periphery. As interstitial
edema becomes more severe, uid can also accumulate in the subpleural space of
the interlobar ssures, causing subpleural stripe or edema, which appears as a thickening of the interlobar ssures on chest radiographs.
As pulmonary venous pressure rises, uid enters the alveolar spaces of the lungs.
Airspace involvement can be detected by poorly dened lung opacities that coalesce
to produce airspace consolidation, which may show air bronchograms. The presence of conuent, cloud-like lung opacities characterizes airspace consolidation.
Airspace consolidation from hydrostatic pulmonary edema is usually bilateral and
symmetric and often has a central or perihilar predominance. However, in some
patients, alveolar pulmonary edema may be asymmetric or atypical in distribution.
Although the appearance of pulmonary edema can vary among different patients,
there is often a similar pattern in an individual patient from episode to episode.
Thus, it is helpful to compare the current radiograph to the one obtained during a
prior episode of pulmonary edema, particularly for patients with an asymmetric or
atypical distribution.
Patients with hydrostatic pulmonary edema often have an enlarged heart, an
increased vascular pedicle width, and pleural effusions. Patients with congestive
heart failure typically have right-sided pleural effusions.
74
ab
Fig. 3.8 Bilateral diffuse
airspace opacication more
likely in keeping
with ARDS
F. Macori
Fig. 3.9 Airspace opacication seen at the chest X-ray (a) conrmed at the CT (b) where a crazy
paving is demonstrated. Bibasal pleural effusion
3.3.2 Acute Respiratory Distress Syndrome
Acute respiratory distress syndrome (ARDS) (Fig.3.8) is a clinical syndrome characterized by hypoxemia resistant to oxygen therapy, absence of clinically apparent
left atrial hypertension, and bilateral pulmonary opacication on the chest
radiograph.
Pulmonary opacities on CT are often more heterogeneous than on the chest
radiograph. A relatively symmetric ground-glass distribution predominates when
ARDS is due to extrapulmonary causes. CT patterns in ARDS may be described as
typical or atypical. Dense consolidation involves the posterior lungs in a dependent
distribution in a typical pattern. Ground-glass opacities are seen in a nondependent
distribution. In the atypical pattern, dense consolidation is seen in nondependent
locations. The atypical distribution of consolidation is more likely to be found
3
The Role of Chest Radiography in the Critical Care Unit
Fig. 3.10 Complete
collapse of the left lung
Fig. 3.11 Right basal
linear atelectasis. The
nasogastric tube is
mispositioned, inserted in
the left bronchus
75
when ARDS is incited by pulmonary disease. Air bronchograms are frequently
seen in both forms. “Crazy paving,” a nonspecic CT appearance of interlobular
septal thickening in a background of ground-glass attenuation, may also be seen
(Fig.3.9).
76
F. Macori
3.3.3 Atelectasis
Atelectasis, a decrease in lung volume, is the most common cause of pulmonary
opacities in the ICU population. It is frequently found after general anesthesia and
thoracic or upper abdominal surgery, occurring in up to 64% of patients in one surgical investigation. Atelectasis is usually subsegmental and can mimic pneumonia,
particularly when signs of volume loss such as crowding of air bronchograms, ssural deviation, mediastinal shift, and diaphragmatic elevation are absent. Flat,
platelike opacities are characteristic of discoid atelectasis. Complete lung collapse,
lobar collapse, or segmental collapse can also be seen (Figs. 3.10 and 3.11).
Atelectasis is categorized (according to mechanism) as obstructive, compressive,
cicatricial, or adhesive. Adhesive atelectasis, common in premature neonates secondary to insufcient surfactant production, is not discussed further.
Obstructive atelectasis is the most common type of atelectasis. Impaired mucociliary function, increased secretions, and altered consciousness are predisposing
factors. When only the distal, small airways are obstructed, crowded air bronchograms are seen. Air bronchograms are absent when the obstruction is more proximal in larger airways. Mucus plugging is a common cause of acute segmental,
lobar, and complete lung collapse. The absence of air bronchograms in patients who
have acute lobar collapse favors mucoid impaction as the etiology and predicts a
higher rate of therapeutic success with bronchoscopy (79–89% in favorable
patients).
Compressive atelectasis is the volume loss secondary to mass effect exerted on
the lung. In the ICU population, pleural uid is usually the cause. Other potential
causes are thoracic tumor, pulmonary abscess, and severe cardiomegaly. Cicatricial
Fig. 3.12 Patchy,
ill-dened ground glass,
mostly on the
dependent zone