key: cord-0036517-g72qaoub
authors: Lohan, Rahul
title: Imaging of ICU Patients
date: 2019-01-15
journal: Thoracic Imaging
DOI: 10.1007/978-981-13-2544-1_7
sha: 1c3cbf2f00f0ff9cc5088200cb12334d15c28ce4
doc_id: 36517
cord_uid: g72qaoub

Imaging in intensive care unit (ICU) is integral to patient management. The portable chest radiograph is the most commonly requested imaging examination in ICU, and, despite its limitations, it significantly contributes to the decision-making process. Multidetector CT (MDCT) is reserved for relatively complex and challenging clinical scenarios. Bedside ultrasound is emerging as a promising imaging modality as it does not subject the patients to risks and resources involved in the transportation of these patients to the CT facility. Ultrasound is an effective modality to triage patients and is being increasingly incorporated into the emergency and intensive care management algorithms.

Imaging in intensive care unit (ICU) is integral to patient management. The portable chest radiograph is the most commonly requested imaging examination in ICU, and, despite its limitations, it significantly contributes to the decisionmaking process. Multidetector CT (MDCT) is reserved for relatively complex and challenging clinical scenarios. Bedside ultrasound is emerging as a promising imaging modality as it does not subject the patients to risks and resources involved in the transportation of these patients to the CT facility. Ultrasound is an effective modality to triage patients and is being increasingly incorporated into the emergency and intensive care management algorithms.

The commonly encountered disease states in ICU setting are pulmonary parenchymal diseases, pulmonary thromboembolism, barotrauma, and pleural fluid. Besides the evaluation of these conditions, imaging is routinely used for the assessment of various catheters and tubes commonly used in ICUs.

The common pulmonary parenchymal disease processes in ICU patients include hydrostatic pulmonary edema, acute respiratory distress syndrome (ARDS), atelectasis, pneumonia, aspiration, and pulmonary hemorrhage.

Pulmonary edema is an abnormal accumulation of fluid in the extravascular compartment of the lungs. The fluid accumulation depends on the capillary permeability and the oncotic pressure, as described by the Starling equation, i.e., Q = K (HPiv − Hpev) − T(OPiv − OPev), where Q represents the amount of fluid filtered and HP and OP denote the hydrostatic and oncotic pressures of the intravascular (iv) and extravascular (ev) compartments. K represents the conductance of the capillary wall, determined by the resistance offered to the water flow by the capillary endothelial cell junctions [1] . T represents the permeability of the capillary membranes to the macromolecules. Lymphatic drainage is another pathway for handling excess water in the lungs. However, the lymphatic drainage needs time to be effective, and in the acute situation, it often fails to eliminate the excess fluid [2] . Classically grouped into cardiogenic and non-cardiogenic variants, the pulmonary edema can be divided into the following four types based on the pathophysiology [3] ( Almost all pulmonary edema presentations in critical care units are due to increased hydrostatic pressure or increased permeability with DAD. The two common pathophysiological forms are further discussed.

The two most common causes of increased hydrostatic pressure edema (HPE) in critical care units are left heart failure and fluid overload. Besides renal and liver failure, overzealous hydration in settings of trauma and immediate postoperative care frequently contibutes to fluid overload. There are two distinct radiological phases of the pressure edema-the interstitial edema and the alveolar edema. The radiographic findings in the early interstitial phase include indistinctness of the intrapulmonary vasculature, peribronchial cuffing, and Kerley lines. Indistinctness of pulmonary vasculature is subtle but often the most useful radiographic sign of early interstitial edema in ICU patients. With increasing intensity and duration of pressure gradient, edema extends into the alveolar spaces, resulting in nodular or acinar areas of increased opacity that coalesce into frank consolidation ( Fig. 7.2 ). There is a good correlation between the increased pressure in the intravascular compartment as measured by the pulmonary capillary wedge pressure (PCWP) and radiographic appearances (Table 7 .1) [4] .

The vascular pedicle width is measured from the SVC and azygos vein complex on the right to proximal descending thoracic aorta on the left. It can provide a reasonable estimate of intravascular volume status. Increased width of vascular pedicle (>7 cm) thus may help in differentiating hydrostatic pulmonary edema from non-cardiogenic edema ( Fig. 7.3) . The CT findings of hydrostatic pulmonary edema include smooth interlobular septal thickening, ground-glass opacities, consolidation, and pleural effusions ( Fig. 7.4) . The distribution of densities often demonstrates gravity-based gradient, with abnormalities being most notable at the lung bases. Atypical distribution or appearances similar to aspiration pneumonitis or pneumonia may be seen in presence of underlying chronic pulmonary disease, such as emphysema [5] .

Acute respiratory distress syndrome (ARDS) represents the most severe form of permeability edema associated with DAD [2, 3] . In ICU settings, the common primary pulmonary pathologies causing ARDS are pneumonia, aspiration, and pulmonary contusions. The common extrathoracic causes include drug toxicity, systemic inflammatory response syndrome, sepsis, shock, and abdominal trauma [5] . Clinically, ARDS is defined by recently created "Berlin defi- (Table 7. 2) [6] . ARDS involves three often overlapping and conflicting stages. The first or exudative stage is characterized by a rapidly progressing high protein content interstitial edema that quickly fills the alveoli and is associated with hemorrhage and hyaline membrane formation. The second or proliferative stage involves organization of the fibrinous exudate, regeneration of the alveolar lining, and thickening of the alveolar septa. The third or fibrotic stage manifests as varying degrees of scarring and formation of subpleural and intrapulmonary cysts. The radiographic findings in exudative phase are that of interstitial edema pattern, rapidly progressing to perihilar opacities and subsequently widespread alveolar consolidation ( Fig. 7.5 ). In comparison to hydrostatic edema, . This gravitational distribution can be changed by patient's position (supine vs prone), suggesting a significant contribution from atelectasis [3] . The atypical pattern comprises of dense consolidation in anterior (in supine position) nondependent locations. This may be seen in up to 5% of ARDS patients and is more common in ARDS with underlying primary pulmonary cause [7] . "Crazy paving," i.e., ground-glass opacities with superimposed inter-and intralobular septal thickening, may be seen [8] .

During the fibroproliferative stage, patchy heterogeneous areas of ground-glass opacification are seen with reticular changes. Traction bronchiectasis and bronchiolectasis may be seen on CT. These findings early in the course of ARDS are associated with a poorer clinical outcome [9] . Subpleural and intrapulmonary cystic lesions may be observed in the fibrotic stage which can directly result in pneumothoraces [9] . Recurrent episodes of exudative phase in the proliferative and fibrotic stages often result in mixed radiologic findings. HRCT of the patients recovered from ARDS on subsequent follow-up shows characteristic anterior lung fibrotic bands with sparing of posterior lungs. Distinguishing imaging features between HPE and ARDS are described in Table 7 .3.

Atelectasis, defined as a decrease in lung volume, is the commonest cause of radiographic parenchymal opacities in ICU patients, particularly amongst the postoperative surgical ICU patients. The atelectasis most commonly involves the left lower lobe (66%), followed by the right lower lobe (22%) and right a b to symmetrical central ground-glass opacities and bilateral pleural effusions at a later stage. Note there is a gravity-based gradient of increasing density in the lungs upper lobe (11%) [10] . Obstructive atelectasis from impaired mucociliary clearance, increased secretions, and altered consciousness is often encountered in the ICU patients. Distal obstruction manifests as crowding of air bronchograms, whereas the proximal mucus plugging leads to lobar or even complete lung collapse ( Fig. 7.8 ). Compressive atelectasis from pleural effusion and cicatrization from fibrosis in later stages of ARDS are other forms of atelectasis seen in ICU setting. The imaging findings include linear, band-like, or wedge-shaped opacities with signs of volume loss. 

Mechanical ventilation and aspiration are two main risk factors for pneumonia in ICU patients. Ventilator-associated pneumonia can occur in up to 24% of patients after 2 days of ventilation [11] . The diagnosis of pneumonia in ICU patients is often challenging as the airspace opacities seen on chest radiographs in these patients can be caused by atelectasis, aspiration, pulmonary hemorrhage, noninfectious lung inflammation (e.g., drug reaction), pulmonary edema, or ARDS [12] . However, there are certain features that may favor pneumonia (Table 7 .4). Air bronchograms typically associated with pneumonia result from the complete filling of the alveolar spaces around nonobstructed bronchi. However, when the airways get filled with mucus, air bronchograms are not seen on imaging which is often the case in critically ill patients (Fig. 7.9 ). On CT, pneumonia can often be differentiated from atelectasis by lack of signs of volume loss. CT may provide additional clues to the possible causative agent of pneumonia. Cavities, upper lobe or superior segment of lower lobe airspace disease, endobronchial spread (tree-in-bud densities), and findings of prior granulomatous disease point toward reactivation tuberculosis (TB). Multiple peripheral lung nodules, solid as well as cavitary, in certain patients (long-term indwelling catheters, endocarditis, or history of IV drug abuse) suggest septic emboli [12] . Widespread bilateral predominantly central ground-glass opacities and cysts with or without spon-taneous pneumothorax in immunocompromised patients are features of Pneumocystis jiroveci pneumonia (PCP), whereas focal areas of consolidation surrounded by a "halo" of groundglass suggest angioinvasive aspergillosis [13] .

Intubation, diminished cough reflex, sedation, altered mental state, and enteric tube feeding predispose the ICU patients to increased risk of aspiration. The different manifestations of the aspiration include chemical pneumonitis, pneumonia, and airway obstruction. Aspiration of large amounts of severely acidic gastric contents can be fatal, resulting in a severe chemical pneumonitis and ARDS [14] .

Aspiration is more common in the right lung, due to the vertical orientation of the right main bronchus. In the supine position, the frequently involved sites are the posterior segments of the upper lobes and superior segment of the lower lobe [12] . The radiographic abnormalities commonly seen with aspiration are patchy ill-defined ground-glass opacities, nodular opacities, or consolidation in the dependent regions of the lungs (Fig. 7.10 ). The opacities usually are seen over the first 1-2 days in aspiration pneumonitis demonstrating relatively rapid resolution on follow up radiographs. Persisting opacities indicate progression to infectious pneumonia, and this is one important reason for following up the patients on radiographs. The CT better demonstrates the ground-glass changes or consolidation. Areas of necrosis and cavitation can be seen when aspirates contain anaerobic organisms [12] . Tree-in-bud opacities present in the abovementioned dependent distribution are also frequently seen with aspiration [8] . 

The pulmonary hemorrhage can be localized or diffuse. The localized form is often secondary to bronchiectasis, tumors, or some infections. The diffuse alveolar hemorrhage results from injury to the alveolar microcirculation leading to bleeding into the air spaces [15] . This form is encountered in various autoimmune diseases, bleeding diathesis, vasculitis, certain drugs, and infections (invasive aspergillosis, mucormycosis). In ICU patients, the culprit drugs often are systemic or catheter-directed thrombolytics (for myocardial infarction, PE, or stroke).

The differentiation of pulmonary hemorrhage from pneumonia or pulmonary edema may be difficult. Rapidly developing central and basilar predominant pulmonary parenchymal opacities sparing the costophrenic angles, along with drop in hemoglobin and hemoptysis (or blood in tracheal aspirate), should suggest the diagnosis of pulmonary hemorrhage. On CT scan, patchy ground-glass opacities, typically cloud-like opacities without significant interlobular septal thickening, are seen in the acute phase. In subacute phase, interlobular and intralobular interstitial thickening often develops [15] . Although the CT imaging features are nonspecific, the distribution of these findings, the temporal evolution of opacities, and the radiologic manifestations of predisposing disease (Table 7 .5) can help in arriving at the diagnosis [15, 16] (Fig. 7.11) . 

The prevalence of pulmonary embolism (PE) in critically ill patients is as high as 27% with only one-third of these cases being suspected clinically [17] . Besides the general risk factors for PE such as obesity, past history of venous thromboembolism, cancer, immobilization, trauma, and recent surgery; the ICU patients are exposed to additional risk factors [18] There are various radiographic signs (Table 7 .6) described for PE [19] [20] [21] [22] . Although these signs are difficult to interpret, their timely recognition might alert the physician to the possibility of PE before it is suspected clinically (Figs. 7.12 and 7.13). CT pulmonary angiography (CTPA) is now the reference standard for diagnosing PE in ICU patients, with most ICUs moving away from the ventilation-perfusion scan and conventional invasive pulmonary angiography. CTPA not only detects PE by direct visualization of the thrombus in pulmonary arteries, it allows risk stratification by providing signs of right heart strain and quantification of thrombus burden. An RV/LV ratio > 0.9-1.5 has been shown to predict adverse outcomes similar to the echocardiographic measurements [23] . Newer CT techniques, such as dual-energy CT, can be used to assess functional lung perfusion [24] as well as reduce contrast burden in ICU patients who are prone to acute kidney injury [25] .

Barotrauma, particularly the pneumothorax, remains a common ICU complication despite continuously improving mechanical ventilation strategies of low tidal volumes and plateau pressures [26] . The other forms of barotrauma are pneumomediastinum, pneumopericardium, pneumoperitoneum, subcutaneous emphysema, and interstitial emphysema. Even a small pneumothorax can rapidly progress to tension pneumothorax in ventilated patients. The typical appearance of a thin curvilinear line, bordered by the lung on one side and pleural air space devoid of lung markings on the other, is often absent in the supine radiographs.

In the supine position, air collects to the least dependent anteromedial pleural space (Fig. 7 .14) resulting in increased radiolucency at the bases and sharply elongated cardiophrenic and costophrenic sulci (the deep sulcus sign) [27] . CT is useful for evaluation of loculated air collections and guides the proper placement of chest tube when pneumothorax persists. Pneumomediastinum (Fig. 7.15 ) in ventilated patients most commonly occurs from the rupture of the terminal airways. The pressure gradient between an alveolus and the interstitium directs the air from the ruptured alveolus to the perivascular and peribronchial fascial sheath. The fascial sheath at the lung root gives away letting the air escape into the mediastinum. With increasing severity, the air overflows into the subcutaneous tissues of the neck and into the retroperitoneum [28] . Pneumomediastinum can also be seen in tracheobronchial injury, following tracheostomy tube placement, asthma, and esophageal rupture.

Pleural effusion in ICU patients is mostly transudative. Despite being a common occurrence, it is difficult to detect small to moderate pleural fluid on the supine radiograph. In addition, differentiating it from other causes of lower zone opacities such as consolidation and atelectasis is often not possible. The costophrenic angle is often not blunted on the a b supine radiograph, and pleural fluid may only demonstrate diffuse hazy "veil-like" opacification from the layering of the pleural fluid (Fig. 7.16 ). The apex is the most dependent location in supine patients and fluid may manifest as an apical cap [29] . CT helps in differentiating pleural fluid from pulmonary parenchymal disease and better demonstrates the loculated pleural fluid collections. On CT, the thick enhancing visceral and parietal pleura suggests empyema often with a "split pleura" sign. Hemothorax is suggested by increased attenuation of the pleural fluid, commonly 35-70 HU [30] . Ultrasound, readily available as a bedside imaging modality in most ICUs, is very useful in demonstrating loculations and in guiding fluid sampling as well a c b 

Tubes, lines, and catheters are always present in ICU radiographs. One major use of the radiographs in ICU is to check their position and to evaluate any complications related to their insertion (Table 7.7) . 

Endotracheal tubes (ETT) are used for short-term respiratory support with mechanical ventilation. The tip of endotracheal tube should be located about 5 cm above the carina when the patient's head is in a neutral position [32] . The neck flexion moves the tube inferiorly by up to 2 cm, and the neck extension moves it superiorly by the same 2 cm, hence the saying "the hose goes with the nose" [5] . Intubation of the main bronchi (most frequently right sided) may result in subsegmental atelectasis (Fig. 7.18 ), segmental collapse, or complete collapse of the contralateral lung and puts the ipsilateral lung at risk of pneumothorax from overventilation. The too high a position of ETT can lead to inadvertent extubation or damage to the larynx. Overinflation of the endotracheal balloon cuff beyond the normal tracheal diameter chronically can lead to tracheal stenosis or may rarely result in acute rupture [33] . The tracheal rupture however mostly occurs in the peri-intubation period, through the membranous trachea within 7 cm of the carina [34] . Difficult intubation can occasionally result in hypopharyngeal injury (Fig. 7.19 ). Tracheostomy tubes are placed when long-term intubation is necessary. The tracheostomy tube tip should be approximately at mid-T3 level. The tracheostomy tube maintains its position during neck movements. Pneumomediastinum can occur following an uncomplicated tracheostomy tube insertion.

Nasogastric tubes are the most commonly used for feeding, medication administration, and suctioning of gastric contents. The tip of a feeding tube should be ideally in the antrum of the stomach or distal to it (post-pyloric) to reduce the risk of aspiration. The proximal side hole of a nasogastric tube should extend beyond the gastroesophageal junction [35] . The bedside chest radiograph is the most important investigation to detect tube malposition. The enteric tubes can coil within the pharynx or esophagus, resulting in high risk of aspiration, or very rarely esophageal perforations. The nasogastric tubes occasionally may terminate in the large airways ( Fig. 7.20) where ectopic feeding can result in direct bronchopulmonary injury, pneumonia, pneumothorax, pulmonary laceration, and pulmonary contusion [5] .

The gastric feeding tubes are easier to insert than small bowel feeding tubes, allowing early initiation of enteral feeds, and are almost always placed at the time of ICU admission. Small bowel feeding tubes (nasojejunal or percutaneous jejunostomy) are reserved for patients who have high gastric residual volumes despite the use of prokinetics [36] . 

The tip of the central venous catheter should be distal to the last venous valve, which is located at the junction of the internal jugular and the subclavian veins. On the CXR, the position of the valve corresponds to the inner aspect of the anterior first rib [35] . A catheter is more likely to get blocked from thrombosis around it when its position is in proximal SVC or at the thoracic inlet than in the distal SVC or at the cavoatrial junction [37] . The inferior border of bronchus intermedius serves as a good guide to the distal SVC ( Fig. 7.21) . On the CXR, the cavoatrial junction corresponds to the lower border of the bronchus intermedius, while the arch of azygos is located at the right tracheobronchial angle a b Azygos location of a catheter tip can be identified by its characteristic orientation and position (Fig. 7.21c Pulmonary artery catheters or Swan-Ganz catheters are placed primarily to measure pulmonary capillary wedge pressure, which helps to differentiate cardiogenic pulmonary edema from non-cardiogenic pulmonary edema. The catheter tip should lie in the main pulmonary arteries or the proximal lobar pulmonary artery (Fig. 7.22) . The catheter tip should not extend beyond the pulmonary hilum on the chest radiograph [38] . A further distal catheter tip increases the risk of arterial injury and pulmonary infarction. Pulmonary infarcts may also occur secondary to persistent balloon occlusion or pericatheter thrombus.

The proper position of the chest tube depends on the contents to be removed from the pleural cavity. The tip of the tube is directed toward the apex for pneumothorax and toward the lung base for fluid drainage (Fig. 7.23 ). The side holes of the chest tube, identified on radiographs as interruptions of the tube's radiopaque line, should lie within the pleural space. An improper location of chest tube results in poor drainage and accumulation of air or fluid in the chest wall. The ineffective drainage may also result from tube kinking; blockage resulting from blood clots, pus, or debris in the tube; and apposition of the tip against the mediastinum [33] . An intrafissural location of the tube may or may not affect its function; however, rarely it may result in herniation of lung parenchyma into the holes of chest tube leading to infarction [39] . Inadvertent parenchymal insertion of a chest tube (Fig. 7.24 ) can lead to pulmonary laceration, hematoma, infarction, and bronchopleural fistula. Besides the lung parenchyma, an inappropriately positioned chest tube can injure the heart, great vessels, diaphragm, liver, and spleen [33] .

Interpretation of ICU radiographs is a challenging task. Important pearls for reporting ICU chest radiographs are summarized in Table 7 .8. 

On the absorption of fluids from the connective tissue spaces

Harrison's principles of internal medicine

Clinical and radiologic features of pulmonary edema

Revisiting signs, strengths and weaknesses of standard chest radiography in patients of acute dyspnea in the emergency department

Intensive care unit imaging

Acute respiratory distress syndrome: the Berlin definition

Acute respiratory distress syndrome caused by pulmonary and extrapulmonary injury: a comparative CT study

Crazy-paving" pattern at thin-section CT of the lungs: radiologic-pathologic overview

Prediction of prognosis for acute respiratory distress syndrome with thin-section CT: validation in 44 cases

Lobar collapse in the surgical intensive care unit

Ventilator-associated pneumonia

Thoracic imaging in ICU

Chest CT for suspected pulmonary complications of oncologic therapies: how I review and report

The many faces of pulmonary aspiration

Diffuse pulmonary hemorrhage: clues to the diagnosis

Manifestations of systemic diseases on thoracic imaging

Venous thromboembolism prophylaxis in critically ill patients

Venous thromboembolic disease: an observational study in medical-surgical intensive care unit patients

On the roentgen diagnosis of lung embolism

Roentgen diagnosis of pulmonary embolism

Pulmonary embolism: roentgenographic and angiographic considerations

Correlation of postmortem chest teleroentgenograms with autopsy findings with special reference to pulmonary embolism and infarction

Prognostic value of echocardiography and spiral computed tomography in patients with pulmonary embolism

Diagnosing pulmonary embolism: new computed tomography applications

Reduced iodine load at CT pulmonary angiography with dualenergy monochromatic imaging: comparison with standard CT pulmonary angiography -a prospective randomized trial

Distribution of pneumothorax in the supine and semirecumbent critically ill adult

Pneumomediastinum revisited

Imaging of the pleura

Complex disease of the pleural space: radiographic and CT evaluation

Stateof-the-art: radiological investigation of pleural disease

Radiographic evaluation of endotracheal tube position

Chest radiography in the ICU: part 1, evaluation of airway, enteric, and pleural tubes

Early radiographic signs of tracheal rupture

Chest radiography in the ICU: part 2, evaluation of cardiovascular lines and other devices

Gastric versus post-pyloric feeding: a systematic review

To clot or not to clot? That is the question in central venous catheters

Lines, tubes, and devices

Lung entrapment and infarction by chest tube suction