Introduction

Rapid interpretation of chest x-rays by intensive care physicians and xsurgeons is essential when treating critically ill patients You should be able to recognize the common normal and pathological appearances of portable chest x-rays in the postoperative or medically xill patient as well as common complications of mechanical lines and their correct positioning

Routine chest films are obtained in the radiology department in a posteroanterior (PA) direction to minimize magnification of the heart The optimal ICU chest x-ray is obtained in the (AP) view at a target-tofilm distance of 72 inches with the patient in the upright position at maximum inspiration; Alternatively a distance of 40 inches is used in the supine patient.

Due to the decreased mobility of patients in the ICU, chest films are often taken while the patient is supine.

The appearance of the chest film is affected by the AP positioning, supine positioning, and the degree of inspiration

PA

AP

   

Have a structured method! Be consistent with that method Dont take short cuts LOOK AT ALL YOUR PATIENTS XRAYS YOURSELF (and with your resident of course!) PRACTICEPRACTICE PRACTICE

SHADOW

Identification!
Correct patient Correct date and time Correct examination

Are old films available? DO THIS EVERYTIME It buys you time and is vitally important.

Projection PA or AP Position Upright or Supine (Supine folks are sick) Inspiratory effort

9-10 posterior ribs thoracic intervertebral disc space just visible medial clavicle heads equidistant to spinous process

Penetration

Positioning/rotation

Maximum x-ray xTransmission (least dense tissue)

Maximum xray x Absorption (densest tissue)

5 9 10

11

Note bilateral flattening of the diaphragms and significant hyperinflation as demonstrated by visualization of 11 posterior ribs.

An inferior anteromedial pneumothorax may be evidenced by delineation of the heart border and a lucent cardiophrenic sulcus. This is the key sign of a pneumothorax as this is the highest point in the supine patient, where the air will accumulate first.

In the supine patient, intrapleural air rises anteriorly and medially, often making the diagnosis of pneumothorax difficult. The anteromedial and subpulmonary locations are the initial areas of air collection in the supine patient. An apical pneumothorax in a supine patient is a sign that a large volume of air is present. Subpulmonic pneumothorax occurs when air accumulates between the base of the lung and the diaphragm. Anterolateral air may increase the radiolucency at the costophrenic sulcus. This is called the deep sulcus sign. Other signs of subpulmonic pneumothorax include a hyperlucent upper quadrant with visualization of the superior surface of the diaphragm and visualization of the inferior vena cava.

Bilateral pleural effusions in a supine patient. This film demonstrates fluid in the posterior basilar space without loss of normal bronchial markings.

A large pleural effusion has wrapped around the lateral and apical lung surfaces

This PA chest film of an erect patient shows a large pleural effusion on the right. Even an effusion this size may be difficult to detect in a supine film

Pleural fluid (arrows) layers out on this left lateral decubitis film

This is a sitting AP film of a patient who underwent abdominal surgery resulting in pneumoperitoneum (arrow). The pneumoperitoneum outlines the inferior border of the diaphram. diaphram. This facilitates identification of the large subpulmonary plueral effusion

Supine radiograph: Sharp diaphragmatic and mediastinal outline

Pulmonary edema occurs when fluid traverses capillary membranes and enters the alveolar space. It is the most common cause of decreased oxygenation in the ICU patient. Three mechanisms lead to pulmonary edema. These are: 1. Increased hydrostatic gradient 2. Diminished oncotic pressure 3. Increased capillary permeability due to endothelial injury Any one or more often a combination of these mechanisms will cause fluid to enter the alveolar space. The causes of pulmonary edema are broadly catogorized as cardiac versus non-cardiac. Poor cardiac function will cause nonincreased hydrostatic pressures in the pulmonary capillary bed resulting in cardiogenic pulmonary edema. Non-cardiogenic pulmonary edema can result Nonfrom volume overload due to renal failure, over hydration, or from diminished oncotic pressure in the liver failure patient, or from endothelial injury as in the patient with ARDS. The radiographic manifestations of cardiogenic edema (much more common) are shon on the next several pages

This is a patient with pulmonary edema with typical bilateral "batwing" increased pulmonary vasculature

This chest film demonstrates cephalization of the pulmonary vessels

congestive heart failure resulting in interstitial edema (left). Notice the Kerley's B lines in the closeup view (right).

Haziness of the pulmonary hila are due to vessel enlargment in a patient with CHF. Air bronchograms are visible ( normally invisible) in he right upper lobe.

Chest Xray PA view on admission shows sharply marginated biconvex opacity in the right interlobar fissure

Cardiac width is larger than half trans-thoracic diameter. Cardiothoraccic rartio >0.5

Vasular phase Cephalization: Vessels in upper chest is more prominent as a manifestation of pulmonary venous hypertension.

Hilar fullness with haziness: Enlarge pulmonary veins with perivascular fluid collection leads to full hazy hilum

Interstitial phase Kerley lines: 2-3 cm long lines in bases perpendicular to pleural surface. Due to increased lymphatic flow and fluid in interstitium

Alveolar phase Basal congestion Pulmonary edema: Bilateral diffuse alveolar findings with butterfly distribution, air bronchograms and soft coalescing densities

Pleural effusions

Rapid changes in CXR

In ARDS the heart is normal in size and there are no pleural effusions. Clinical setting and the wedge pressure are necessary in some cases. cases. While cardiogenic pulmonary edema typically begins centrally in the bilateral perihilar areas, ARDS usually causes more uniform opacification. Pleural effusions are not typical of ARDS but often present in CHF. Kerley B lines are common in CHF but not in ARDS, while air bronchograms can be found in both.

The progression of this patients pulmonary disease is consistent with ARDS

Causes of pneumomediastinum include; asthma, surgery (post-op complication), traumatic tracheobronchial rupture, abrupt changes in intrathoracic pressure (vomiting, coughing, exercise, and parturition), ruptured esophagus, barotrauma, and smoking crack cocaine. Pneumomediastinum should be distinguished from pneumopericardium and pneumothorax. In pneumopericardium, air can be present underneath the heart, but does not enter the neck

Air density within the pericardium (arrows) after aspiration of a large pericardial effusion

A lucent stripe along the inferior border of the cardiac silhouette which crosses the midline is also diagnostic for pneumopericardium. pneumopericardium.

Right mainstem bronchus intubation (arrow) leading to left lower lobe collapse (arrow heads).

This patient had a large right pleural effusion (left) which had been evacuated 12 hours later (right) by a pigtail thoracostomy tube

This chest tube failed to remove the pleural effusion due to anterior placement

Central venous catheter tip (small arrow) at junction of left subclavian vein and superior vena cava (arrow).

Intracardiac placement of a central venous catheter (arrow). The tip (small arrow) is within the right ventricle..

Close up view of chest x-ray showing catheter tip in the external jugular vein. xEach catheter should be followed to its tip so that an abnormality like this one on the edge of the film is not missed.

Single lead pacer with tip in the right ventricle.the tip should be at the apex with no sharp angulations throughout its length tip should be imbedded within the cardiac trabeculae( it appears 3 to 4 mm beneath the epicardial fat stripe.)

Pleural effusion Pneumothorax Hemothorax Pulmonary embolus Trauma Monitoring chest drainage TB

Lung cancer Chest pain (MI?) Hypertension Screening Pneumonia COPD Asthma

Compare symmetry Review organs (bones, lungs, heart) in sequence Left to Right then Top to Bottom Random free search

Recognition of abnormal first requires knowledge of normal. Over diagnosis of normal variation may be more serious than omission & may lead to needless & harmful therapy.

 

Is heart enlarged or normal? Signs of heart failure and fluid overload? Does patient have pneumonia or collapsed lung? Is there evidence of emphysema? Are there findings of an aortic aneurysm? Is there fluid in the sac that surrounds the lung? Is there free air under the diaphragm? Is there a tumor in the lung that could represent cancer?

Systematically evaluate chest wall, mediastinum, lungs, pleural space, heart, large arteries, ribs & diaphragm. Also evaluate neck, axilla, thyroid gland & abdomen

What does air under diaphragm signify? What is best position for this diagnosis?

You can recognize air, water & bone density on chest x-ray Lung fields appear dark because of air.

99% of the lung is air.

The pulmonary vasculature, interstitial space, constitutes 1% of the lung Gives a lacy lung pattern. Most disease states replace air with a pathological process which usually is a liquid density and appears white.

Supine position

Decreases lung volume, increased heart size Basilar infiltrates & interstitial spaces accentuated Increases venous return to the heart Enlarges normal structures Changes air-fluid levels Lung structures & diaphragm blurred Basilar infiltrates & interstitial spaces accentuated Increased heart size

Semi-upright position

Failure to hold breath

Expiration film

10% of all x-ray interpretations have errors

What is wrong with this lung tissue???

Nothing!! But the clavicle is fractured!

Especially if there are multiple problems, dont focus on the most obvious abnormality!

IDENTIFICATION
Correct patient Correct date & time Correct examination Right vs. Left side Comparison film

TECHNIQUE

Complete exam? All views Entire anatomical area included?

Projection
Is the film AP or PA? The width of heart & mediastinum larger on AP film

Position

TECHNIQUE, cont.

TECHNIQUE, cont.


Penetration Over-penetrated dark films can obscure subtle pathologies Under-penetrated white films may given impression of diffuse increased density

Inspiration  Normal, erect, inspiratory CXR shows 9.5-10.5 ribs.  Less inspiration appears diffusely denser  Diaphragms elevated causing heart & mediastinum to appear enlarged

    

Order of exam is important. Start with "less significant" Tendency to stop looking as soon as find pathology Identify atelectasis behind heart shadow! Dont notice tip of ET tube is in right main stem bronchus, causing the atelectasis!

TECHNIQUE, cont.


Rotation  Determined by distance between spinous process & medial clavicle  Affects heart size & shape, aortic tortuosity, mediastinal widening, density of lung fields

INTERPRETATION


Extraneous material  Contrast  Lines, tubes, clips  All properly located?

INTERPRETATION


Bones  Fracture, dislocation  Mineralization

Soft tissues
Asymmetry  Calcifications


Lung fields
Asymmetry  Consolidation  Nodules, lesions


Diaphragms & Below

Free air  Dilated bowel  Abnormal position


Heart
Size & shape  Cardiothoracic ratio


INTERPRETATION


INTERPRETATION


Mediastinum  Width  Masses  Contour

Pulmonary vascularity  Taper at periphery  Narrow toward upper lobes with erect film  Asymmetry

Hila
Asymmetry  Vessel aneurysm  Trachea & carina


Interstitial markings
Very fine  If indistinct, prominent suspect edema, fibrosis


Alveolar space filled with inflammatory exudate

WBC, bacteria, plasma, and debris

Increased heart size: cardiothoracic ratio >0.5

Large hila with indistinct markings Fluid in interlobar fissures Pleural effusions, alveolar edema

Congestion Interstitial and alveolar edema Collapsed or distended alveoli Bilateral

Granulomatous Inflammation Bilateral & symmetrical hilar & mediastinal LAD Generalized fibrosis

No ventilation to lobe beyond the obstruction Trapped air absorbed by pulmonary circulation Segmental/lobar density Compensatory hyperinflation of normal lungs.