💀CRX Flashcards
- Firsts, 3. Quality, 4. Airway, 5. Bone, 6. CadioMediastinum 7. Diaohragm, 8. Effusions (Pleural, pericardial), 9. Fields (lung), 10. Pneumonia, 13. Groung glass, SPN, TB, PH, PE, Pneumo, IPF, emohysema, Mediastinal mass, pneumopericardium, dia hernia, hilar adenopathy, LC, abscess, tubes lines drains, pleural effusion, pericardial effusion, pulmonary edema, cadiogenic edema, CHF, cephalization, kerley b, interstitial edema, air bronchogram, alveolar edema, ARDS, atelectasis, 64., 67. aspiration syndromes
Index
Firsts
Turn off stray lights, optimize room lighting, view images in order
Patient data:
Name
Date
PA/AP
Uprigt/supine
Quality
Rotated?
Penetration? (Thoracic spine seen through heart)
All areas included (costophrenic angles)
Inflation (3 cm diaphragmatic curvature; 8 -10 posterior ribs in nl)
Airway
Deviation of the trachea (related to a mediastinal hematoma)
Masses in the airway
Airway compression
Bone
Lesions or fractures
Clavicles
Soft tissue calcification
RUG (gallstones, free air)
CardioMediastinum
Cardiothoracic ratio
RA, LV, LA
Mediastinal contour: width? mass?
Lines (R paratracheal, Azygous, SVC, Aorta, Azygoesophageal line, descending aortic line)
Widened mediastinum:
Loss of the normal clear aortic arch contour “knob”
Loss of the appearance of a normal descending thoracic aorta (no ‘lateral aortic silhouette’ is seen).
Deviation of nasogastric tubes to the right (Indicating a mediastinal hematoma pushing the esophagus to the right side).
Left apical pleural ‘capping’
There is is a rind of fluid above the left lung apex where blood has tracked posteriorly over the left apex.
Signs of a supine pleural effusion
5 T’s Thymoma, teratoma, thyroid, traumatic aorta, ?
Diaphragm
Sharp border
Costophrenic angles sharp bilaterally
Air under diaphragm
Effisions (Pleura, Pericardial)
Lucencies (pneumothorax)
Thickeing, nodularity, calcification, or effusions
Fields (Lung)
Lung zones symmetrical?
Parenchyma (focal or diffuse abnormalitis)
Interstitial and vascular markings (size, prominence)
Lucency (pneumothorax), cavity, or abnormal shadowing (companion shadow of the second rib)
Hila (l higer than right; branching pattern)
Solitary Pulmonary Nodule
A differential of possible etiologies is as follows:
Granuloma – usually caused by fungal infections like histoplasmosis or tuberculosis
Lung Carcinoma
Solitary metastasis – usually from colon, breast, kidney, ovary, or testis
Round pneumonia
Abscess
Round atelectasis
Hamartoma – popcorn calcification is sometimes seen
Sequestration
Arteriovenous malformation
Other things can cause an apparent nodule but are actually outside the lung including:
Fluid in an interlobar fissure
Pleural plaques – small, often calcified, plate-like surfaces on the pleura often caused by asbestos fibers that invade the pleura from the lungs
Skin lesions – nipple shadow, mole, lipoma, etc.
Low Risk Patient
≤ 4mmNo follow-up needed
4-6mm12 mo; if no change - stop
6-8mm6-12 mo; no change - follow-up at 18-24 mo
> 8mmCT follow-up at 3, 9, 24mo or PET/CT, or biopsy
High Risk Patient (eg. smoking history or history of malignancy)
≤ 4mm 12 mo; if no change - stop
4-6mm 6-12mo; no change - follow-up at 18-24 mo
6-8mm 3-6mo; no change - follow-up at 18-24 mo
> 8 mm CT; follow-up at 3, 9, 24mo or PET/CT, or biopsy
An initial CT scan will also help evaluate whether the lesion can be accessed percutaneously without risk for pneumothorax.
Percutaneous biopsy is recommended for lesions that appear malignant and in patients with high clinical suspicion for malignancy. If the CT findings are suspicious for malignancy, a biopsy can be attempted by CT guidance.
Post-primary TB:
Focal patchy airspace disease “cotton wool” shadows, cavitation, fibrosis, nodal calcification, and flecks of caseous material. These occur most commonly in the posterior segments of the upper lobes, and superior segments of the lower lobes.
Pulmonary hemorrhage:
Blood fills the bronchi and eventually the alveoli.
Has an appearance like that of other airspace filling processes (pneumonia, edema) which have opacity often with air bronchograms.
Caused by trauma, Goodpastrue’s syndrome, bleeding disorders, high altitude, and mitral stenosis.
Notable in that it may clear more quickly than other alveolar densities such as pneumonia.
Pneumomediastinum
In the intubated patient the most likely source of air in the mediastinum is pulmonary interstitial air dissecting centripetally. Air in the mediastinum may also originate from tracheobronchial injury or air dissecting through fascial planes from the retroperitoneum. A sudden increase in thoracic pressures (e.g. blunt trauma) may also cause alveolar rupture and consequently pneumomediastinum.
Findings include; streaky lucencies over the mediastinum that extend into the neck, and elevation of the parietal pleura along the mediastinal borders.
Pneumomediastinum often dissects up into the neck. This helps to distinguish it from pneumopericardium that, unlike pneumomediastinum, can extend inferior to the heart.
Causes of pneumomediastinum include; asthma, surgery (post-op complication), traumatic tracheobronchial rupture, abrupt changes in intrathoracic pressure (vomiting, coughing, exercise, 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.
Continuois diaphram sign
Pneumomediastinum generally will not develop clinical manisfestations. However, a retrosternal crunch is sometimes auscultated (Hamman’s crunch).
Pneumomediastinum rarely causes tension pericardium due to the compressibility of air and the fact that rarely is the pneumomediastinum non-communicating tension due to air is rare. Pneumomediastinum may cause pneumothorax (the reverse is not true) or pneumoperitoneum.
Interstitial pulmonary fibrosis
The six most common causes of diffuse interstitial pulmonary fibrosis are idiopathic (IPF, >50% of cases), collagen vascular disease, cytotoxic agents and nitrofurantoin, pneumoconioses, radiation, and sarcoidosis. Clinically the patient with IPF will present with progressive exertional dyspnea and a nonproductive cough. Radiographically, IPF is associated with hazy “ground glass” opacification early and volume loss with linear opacities bilaterally, and honeycomb lung in the late stages. IPF carries a poor prognosis with death due to pulmonary failure usually occurring within 3-6 years of the diagnosis unless lung transplant is performed.
Emphysema
Loss of elastic recoil of the lung with destruction of pulmonary capillary bed and
Commonly seen on CXR as diffuse hyperinflation with flattening of diaphragms, increased retrosternal space, bullae (lucent, air-containing spaces that have no vessels that are not perfused) and enlargement of PA/RV (secondary to chronic hypoxia) an entity also known as cor pulmonale. Hyperinflation and bullae are the best radiographic predictors of emphysema. However, the radiographic findings correlate poorly with the patientâs pulmonary function tests. CT and HRCT (high resolution CT) has emerged as a technique to evaluate different types, panlobular, intralobular, paraseptal and for guidance prior to volume reduction surgery.
Occasionally the trachea is very narrow in the mediolateral plane in emphysema. “Saber sheath” tracheal deformity is when the coronal diameter is less than 2/3 that of the sagittal.
In smokers with known emphysema the upper lung zones are commonly more involved than the lower lobes. This situation is reversed in patients with alpha-1 anti-trypsin deficiency, where the lower lobes are affected.
Chronic bronchitis commonly occurs in patients with emphysema and is associated with bronchial wall thickening.
alveolar septa.
“loculated”
Pneumopericardium
Pneumopericardium, an uncommon occurence, is most often found in the post-operative cardiac patient. Radiographically, pneumopericardium appears as a lucent area around the heart extending up to the main pulmonary arteries.
A lucent stripe along the inferior border of the cardiac silhouette which crosses the midline is also diagnostic for pneumopericardium “continuous diaphragm sign”
Endotracheal tubes (ET Tubes) or tracheostomy tubes
Cuffed conduits placed in the trachea either through the oropharynx or through a surgically created tracheostomy. These tubes maintain airway patency and allow for mechanical ventilation of patients with respiratory failure. A tracheostomy is generally performed in patients who are intubated for longer than 1-3 weeks or who have upper airway obstruction.
The carina can be assumed to be at the T4-T5 interspace, given that 95% of patients’ carinas project over the T5, T6, or T7 vertebral bodies.
The Dee method for approximating the position of the carina involves defining the aortic arch and then drawing a line inferomedially through the middle of the arch at a 45 degree angle to the midline. The intersection of the midline and the diagonal line is the most likely position of the carina.
Approximately, 10% of endotracheal tubes are malpositioned. The tube is more likely to enter the right main stem bronchus, due to its more vertical orientation, and reduce left lung ventilation, leading to collapse of the left lung. If the endotracheal tube enters into the bronchus intermedius, the right upper lobe can also collapse. Superiorly placed ET tubes may enter the pharynx or dislodge from the trachea into the esophagus causing filling of the stomach with air and, potentially, reflux of gastric contents. The glottis may also be damaged.
Major complications from endotracheal tubes are unusual. These include tracheal stenosis, tracheal ruputure, cord paralysis, cervical mediastinal emphysema, hematoma, and abscess formation.
Nasogastric and Feeding Tubes
Inserted through the nares and into the stomach. They are used for gastric decompression or feeding. Generally a chest x-ray is not necessary following the placement of a nasogastric tube.
Feeding tubes are generally placed into the proximal small bowel, as confirmed by an abdominal film. A chest x-ray may be obtained following the insertion of small-bore feeding tubes to rule out placement within the lung, which may have serious consequences. Also, patients who are status-post esophagectomy should receive a chest x-ray to evaluate the placement of any nasogastric tube.
Central Venous Pressure Monitors (line)
The intravascular volume status of critically ill patients is crucial to their management. A central venous pressure can be obtained directly via central vein catheters placed either through the subclavian veins or the internal jugular veins. Similarly, intravenous catheters may be used to infuse large volumes over longer periods of times with little chance of thrombosis.
Proper placement of central venous pressure monitors is necessary for accurate measurements. Ideally the catheter tip should lie between the most proximal venous valves of the subclavian or jugular veins and the right atrium.
Usually the last valve in the subclavian vein is at the level of the anterior portion of the first rib. Therefore, the tip should be medial to this point. (2.5 cm from where they join to form the brachiocephalic vein).
The most common locations for malpositioned catheters include the internal jugular vein, right atrium, and right ventricle. Arrhythmias or cardiac perforations may result from placement of lines within the heart.
Complications of central line placement may result in pneumothorax, occurring in as many as 6% of cases.
Swan-Ganz catheters (pulmonary capillary wedge pressure monitors)
Used to measure pulmonary wedge pressures. These catheters allow the intensivist to have an accurate measurement of the patient’s volume status and can help differentiate between cardiac and non-cardiac pulmonary edema.
Pulmonary capillary wedge pressure catheters (PCWP) are introduced percutaneously into the venous system. They are advanced through the right heart and into the pulmonary artery. A balloon at the end of the catheter is then inflated causing the tip of the catheter to be wedged into a branch of the pulmonary artery. The tip is “floated” to a distal pulmonary artery and wedged there. Once the tip is wedged, the balloon should be deflated. Once a reading is obtained, the tip is pulled back to the main pulmonary artery. The catheter tip should ideally be positioned no more distally than the proximal interlobar pulmonary arteries. A good rule of thumb is that the catheter tip should be within the mediastinal shadow. Placement more distally increases the chance of pulmonary infarction or vessel rupture.
Malpositioning of PCWP catheters is exceedingly common, found in approximately 25% of catheters placed. This may lead to false readings and an increased risk for complications. Complications of PCWP catheter placement include pneumothorax, pulmonary infarction, cardiac arrhythmias, pulmonary artery perforation, endocarditis, and sepsis.
Intraaortic counterpulsation balloon pump (IACB)
Used to decrease afterload and increase cardiac perfusion in patients with cardiogenic shock. The IACB is synchronized with either the aortic pressures or the patient’s EKG to inflate during diastole and deflate during systole. Generally, the IACB is introduced percutaneously through the right femoral artery. Proper positioning of the IACB is critical to prevent occlusion of major vessels. Ideally the catheter should be in the region of the aortic isthmus or left main bronchus and above the origins of the celiac trunk and superior mesenteric artery. During systole the balloon may appear as a fusiform air (helium) containing radiolucency.
Transvenous Pacing Device
Patients in the ICU with bradyarrhythmias or heart block may require cardiac pacing. Transvenous pacers are introduced through the cephalic or subclavian vein into the apex of the right ventricle. Frontal and lateral projections are required to evaluate pacemaker placement. In the frontal view, the pacer tip should be at the apex with no sharp angulations throughout its length. On the lateral view, the tip should be imbedded within the cardiac trabeculae in such a way that it appears 3 to 4 mm beneath the epicardial fat stripe. A tip which appears beyond the epicardial fat stripe may have perforated the myocardium. Pacers placed within the coronary sinus will appear to be directed posteriorly on the lateral chest x-ray. The integrity of the pacer wire should be inspected along its entire length.
Adult respiratory distress syndrome (ARDS)
ARDS is a term used to describe a constellation of clinical and radiographic signs and symptoms reflecting pulmonary edema in the absence of elevated pulmonary venous pressures. ARDS is relatively common in the ICU population and is associated with high mortality (~50%). The syndrome results from a variety of causes, including sepsis or pulmonary infection, severe trauma, and aspiration of gastric contents, all of which together account for 80% of cases. Whatever the initial cause, all share activation of the complement pathway with damage to the alveolar capillary endothelium, increased vascular permeability, and subsequent development of first interstitial and then alveolar pulmonary edema. Clinically, there is severe respiratory distress characterized by marked hypoxia that responds poorly even to administration of high concentrations of oxygen. Pulmonary capillary wedge pressure is usually normal. Decreased surfactant production leads to poor lung compliance and atelectasis that results in an intrapulmonary shunt with perfusion but no effective ventilation. Positive End Expiratory Pressure (PEEP) can help to decrease atelectasis, shunting while improving oxygenation. Patients surviving the syndrome may progress to pulmonary fibrosis or have no sequelae. The longer and more severe the ARDS, the more likely are long term consequences. Other factors may also contribute, such as age and preexisting COPD.
Atelectasis
Atelectasis is a term used to describe reduced inflation in part of the lung.
Atelectasis in ICU patients occurs most frequently in the left lower lobe, presumably due to compression of the lower lobe bronchus by the heart, in the supine patient. Contributing to this tendency is the relatively greater difficulty of blind suctioning of the left lower lobe. The etiology of atelectasis includes any process which reduces aveolar ventilation including general anesthesia, splinting from pain following surgery, or bronchial obstruction by mucus plugging. Mobilization of secretions may be inhibited by inflammatory lung disease, edema, or tracheal intubation. The final result is reduced alveolar distention resulting in decreased surfactant production which propagates the ateletasis further. Usually atelectasis is more extensive than is suggested by the radiograph. Extensive alveolar hypoventilation may result in an effective right to left shunt and subsequent hypoxia. Atelectasis is reversible and preventable with the use of hyperventilation and incentive spirometry especially in the post-operative period.
Is most often caused by an endobronchial lesion, such as mucus plug or tumor. It can also be caused by extrinsic compression centrally by a mass such as lymph nodes or peripheral compression by pleural effusion. An unusual type of atelectasis is cicatricial and is secondary to scarring, TB, or status post radiation.
Atelectasis is almost always associated with a linear increased density on chest x-ray. The apex tends to be at the hilum. The density is associated with volume loss. Some indirect signs of volume loss include vascular crowding or fissural, tracheal, or mediastinal shift, towards the collapse. There may be compensatory hyperinflation of adjacent lobes, or hilar elevation (upper lobe collapse) or depression (lower lobe collapse). Segmental and subsegmental collapse may show linear, curvilinear, wedge shaped opacities. This is most often associated with post-op patients and those with massive hepatosplenomegaly or ascites .
Radiographically, atelectasis may vary from complete lung collapse to relatively normal-appearing lungs. For example, acute mucus plugging may cause only a slight diffuse reduction in lobar or lung volume without visible opacity. Nevertheless, the physiologic effects can be significant. In the so called mucus plugging syndrome, the association of sudden hypoxia with a normal or quasi-normal chest radiograph can lead to the suspicion of a pulmonary embolus. Mild atelectasis usually takes the form of minimal basilar shadowing or linear streaks (subsegmental or “discoid” atelectasis) and may not be physiologically significant. Atelectasis may also appear similar to pulmonary consolidation (dense opacification of all or a portion of a lung due to filling of air spaces by abnormal material), making it difficult to distinguish from pneumonia or other causes of consolidation. The distinction between atelectasis and other causes of consolidation is important, and certain clues exist to aid in making that determination. Atelectasis will often respond to increased ventilation, while pneumonia, for example, will not. Crowding of vessels, shifting of structures such as interlobar fissures towards areas of lung volume loss and elevation of the hemidiaphragm suggests atelectasis. Another key for distinguishing between atelectasis and consolidation is recognition of the typical patterns that each pulmonary lobe follows when collapsing.
Right Upper Lobe Atelectasis
Right upper lobe atelectasis is easily detected as the lobe migrates superomedially toward the apex and mediastinum. The minor fissure elevates and the inferior border of the collapsed lobe is a well demarcated curvilinear border arcing from the hilum towards the apex with inferior concavity. Due to reactive hyperaeration of the lower lobe, the lower lobe artery will often be displaced superiorly on a frontal view.
Left Upper Lobe Atelectasis
The left lung lacks a middle lobe and therefore a minor fissure, so left upper lobe atelectasis presents a different picture from that of the right upper lobe collapse. The result is predominantly anterior shift of the upper lobe in left upper lobe collapse, with loss of the left upper cardiac border. The expanded lower lobe will migrate to a location both superior and posterior to the upper lobe in order to occupy the vacated space. As the lower lobe expands, the lower lobe artery shifts superiorly. The left mainstem bronchus also rotates to a nearly horizontal position.
Right Middle Lobe Atelectasis
Right middle lobe atelectasis may cause minimal changes on the frontal chest film. A loss of definition of the right heart border is the key finding. Right middle lobe collapse is usually more easily seen in the lateral view. The horizontal and lower portion of the major fissures start to approximate with increasing opacity leading to a wedge of opacity pointing to the hilum. Like other cases of atelectasis, this collapse may by confused with right middle lobe pneumonia.
Left Lower Lobe Atelectasis
Atelectasis of either the right or left lower lobe presents a similar appearance. Silhouetting of the corresponding hemidiaphragm, crowding of vessels, and air bronchograms are standard, and silhouetting of descending aorta is seen on the left. It is important to remember that these findings are all nonspecific, often occuring in cases of consolidation, as well. A substantially collapsed lower lobe will usually show as a triangular opacity situated posteromedially against the mediastinum.
Right Lower Lobe Atelectasis
Silhouetting of the right hemidiaphragm and air bronchograms are common signs of right lower lobe atelectasis. Right lower lobe atelectasis can be distinguished from right middle lobe atelectasis by the persistance of the right heart border.
Aspiration Syndromes
ICU patients are at risk for aspiration pneumonitis. Reduced consciousness, neuromuscular disorders, and intratracheal or intraesophageal devices all are factors which may predispose patients to aspiration by compromising the patient’s airway defense mechanisms.The effects of aspiration are determined by volume of the aspirate and the nature of the aspirated material. These determine the extent and severity of any inflammatory response. Chemical irritants may be acid, alkali or paticulate in nature depending on gastric contents.
Aspiration of gastric acid is also known as Mendelson’s Syndrome, it is the most common type of aspiration. The degree of irritation to the lung is directly dependent on the acidity and volume of the aspirated fluid. The lung responds to pH < 2.5 with severe bronchospasm and the release of inflammatory mediators. The initial result is a chemical pulmonary edema. Secondary infection may or may not result. The clinical manifestations occur within minutes of the event and include cough, dyspnea, wheezing and diffuse crackles. Fever and an elevated white count will occur in the majority of patients. The consequences of aspiration range from shock to uncomplicated resolution of the initial event. The chest film in patients that progress to pneumonitis will reveal pulmonary consolidation within the first two days. The consolidation is usually perihilar and bilateral, though asymmetric. The radiographic findings begin to stablize or resolve by the third day. Some patients’ radiographs will show worsening of the consolidation as well as findings associated with pneumonia, including pleural effusions and abscess formation. Aspiration may also cause ARDS.
