Acute Pulmonary Changes

Acute Diffuse Linear, Reticular, Reticulonodular (Interstitial) Pattern

Acute Diffuse Interstitial Pattern

Checklist:

Are the increased markings linear, reticular, or made up of small nodules?

Are they associated with segmental or lobar consolidation?

Do the vessels appear unsharp or enlarged cranially? Can you detect air bronchograms? Are the increased lung markings more evident centrally or basally?

Are there areas of increased radiolucency and decreased vascularity?

Are the bronchi dilated, their walls thickened?

Is the heart enlarged?

Are the hila plump in appearance?

Patterns of Evil

David Shortbreath (57) has been brought to the emergency room. He has had chest pain at work several times over the past few weeks; it has been just absolutely awful because he felt severely short of breath at the same time. His colleagues at the construction site grabbed him, sat him in the car, and rushed him to the hospital, breaking all speed limits on the highway. During that ride Mr. Shortbreath could breath in more easily when he held his head out of the window and breathed against the airstream with his mouth open. Now the ER docs are taking care of him, studying the laboratory parameters and getting an ECG. A chest radiograph is also done (Fig. 6.32). Paul stands close to the lightbox to get a quick first glance at the image.

^ What Is Your Diagnosis?

Left ventricular failure with pulmonary venous congestion: Pulmonary venous congestion is a typical consequence of left ventricular dysfunction, for example, after coronary infarction. The mounting pulmonary venous pressure is reflected on the CXR by a number of specific findings:

• Pulmonary venous redistribution: The first reaction of the pulmonary vasculature to an increase in vascular pressure is to make use of the vessels' reserve capacity. In this process the blood is redirected from the basal lung vessels, which normally hold more blood owing to the hydrostatic pressure gradient, to the cranial pulmonary vessels (see Fig. 6.1). This phenomenon is also called pulmonary venous redistribution.

I The Case of David Shortbreath

Pulmonary Vasculature Cxr
Fig. 6.32 Have a look at the CXR of Mr. Shortbreath. What are the pertinent findings?

f The normal size relation of the basal to the cranial vessel i calibers is about 2 :1 (at identical distance from the hilum).

The basal vessels may even contract a little during this process. Naturally these changes are only noticeable if the patient is upright at the time the CXR is taken (hydrostatic pressure!) (Fig. 6.33). In the recumbent patient the pulmonary venous redistribution cannot be diagnosed because the vessel calibers even out; the vector of the hydrostatic pressure gradient has now changed to the anterior-posterior direction, which is not visible on a frontal supine radiograph (see Fig. 6.3)!

• Fluid exudation into the interstitium: If the reserve capacity of the vessels is exhausted, fluid begins to leak into the interstitium. This process can be observed on the CXR if one looks for these four different structures:

1. The interlobular septae: Fluid in the radially oriented interlobular septae is best appreciated where the septae are parallel to the x-ray beam and where they cannot be mistaken for vessels. This is the case in the peripheral 1 cm of the parenchyma of the lung where vessels are so small that they are beyond the limits of radiographic

Normal Erect Cxr Images
Fig. 6.33 a On the left you see a normal chest exposed in the standard erect position. Compare the vessel calibers at the same distance to the hilum both at the lung base and apex. The size relation of the basal vessels in comparison to the upper lobe vessel is about 2:1. On the right, the same

visualization. The resulting linear structures on the CXR are called Kerley lines: Kerley B in the basal periphery (these are the most important ones, Fig. 6.34a) and Kerley A in the cranial periphery. If the thickening is so pronounced that it becomes visible as a reticular pattern in the central perihilar lung, this is called the Kerley C pattern. Kerley C lines are rarely seen in pulmonary venous congestion but do occur when the interstitium is infiltrated by malignant cells. This dreaded but frequent complication of, for example, advanced breast carcinoma is called lymphangitic spread or carcinomatosis (Fig. 6.34b).

2. Fissures: Interlobar fissures are made up of two layers of pleural lining and thus two layers of interstitium as well. Furthermore, a little fluid may enter the pleural space between the two pleural linings. If the fissures appear particularly prominent or thickened on the CXR, the reason may be fluid overload in the interstitial space (Fig. 6.34a).

3. Bronchial wall: The thickness of the interstitium can also be evaluated by looking at the walls of the larger bronchi in the neighborhood of the hilum that are running parallel to the x-ray beam and therefore appear b

Interlobar Septae

volunteer has changed body orientation, with a subsequent redistribution of the pulmonary perfusion. Check the vessel calibers!

b The documented position is not unusual at large academic institutions and reverses the natural hydrostatic pressure gradient.

I Upper Lobe Pulmonary Venous Redistribution

Kerly Lines

I Kerley Lines a Kerley B lines a Kerley B lines

Kerley Lines

Fig. 6.34 a On the left you see a section of a CXR in severe lung edema. Note the thickening of the minor fissure (black arrow) and the horizontal interlobular septae (white arrow) in the pulmonary periphery. Vessels do not normally show in this parapleural stripe. Compare to a normal section below.

b On the left is a section of an erect CXR. The lung interstitium with the vessels, bronchi, and the surrounding fibrous tissue is irregular, micronodular, and reticular in pattern. This is a case of lymphangitic carcinomatosis in a breast cancer patient. The tumor cells grow along the interstitium and form knotty cell nests. Compare to a normal anatomy below.

Fig. 6.34 a On the left you see a section of a CXR in severe lung edema. Note the thickening of the minor fissure (black arrow) and the horizontal interlobular septae (white arrow) in the pulmonary periphery. Vessels do not normally show in this parapleural stripe. Compare to a normal section below.

b On the left is a section of an erect CXR. The lung interstitium with the vessels, bronchi, and the surrounding fibrous tissue is irregular, micronodular, and reticular in pattern. This is a case of lymphangitic carcinomatosis in a breast cancer patient. The tumor cells grow along the interstitium and form knotty cell nests. Compare to a normal anatomy below.

4. Vascular wall: Naturally, the same occurs in the vessel walls but it cannot be observed that well. (Do you know why?) Eventually the caliber of the vessels increase and their contours become hazy (Fig. 6.35).

• Fluid leaking out of the interstitium into the alveolar space: If the pulmonary venous pressure remains high or continues to increase, the interstitial lymph drainage is eventually overwhelmed and the fluid is pressed into the alveoli. The subsequent corresponding radiographic pattern is that of patchy and confluent density; this is also called an alveolar pattern. Radiographically the lung tissue now appears much denser than the bronchi, which is why they now become visible against the backdrop of the alveoli. This phenomenon is also called "air-bronchogram" and is typical for alveolar disease (Fig. 6.36a). Frequently, fluid exudation begins in the perihilar region and then expands toward the periphery. It may do so simultaneously in both lungs, sparing the lung periphery: a "butterfly distribution" or "bat's wing" pattern (Fig. 6.36b) results that is the hallmark of severe alveolar edema. In patients who are severely compromised, perhaps in the intensive care unit, who have been lying on one side for a prolonged period of time, the distribution of alveolar fluid may be asymmetric. Furthermore, patients with severe inhomogeneously distributed bullous emphysema can only produce the radiographic appearance of alveolar edema in the "good" portions of their lung, because the remainder of the lung is made up of large air-filled spaces with very few if any blood vessels.

I Acute Alveolar Pulmonary Edema a "Air bronchogram" b "Butterfly or batwing edema"

a "Air bronchogram" b "Butterfly or batwing edema"

Bronchial Alveolar Cuffing
Fig. 6.36 a If the bronchial tree can be traced from the hilum to the central lung parenchyma, this is also called "air bronchogram." b The edema spares the lung periphery initially. The typical butterfly or batwing configuration results.

I "Bronchial Cuffing"

I "Bronchial Cuffing"

Batwing Lung Appearance

Fig. 6.35 Bronchus and artery appear in a typical "number 8" configuration when imaged head-on or "down the barrel." The bronchial wall normally does not exceed 1 mm (left section, arrow). In pulmonary edema the thickness of the interstitium around the bronchial wall and the artery increases (right section, arrow) rendering their contours unsharp.

Fig. 6.35 Bronchus and artery appear in a typical "number 8" configuration when imaged head-on or "down the barrel." The bronchial wall normally does not exceed 1 mm (left section, arrow). In pulmonary edema the thickness of the interstitium around the bronchial wall and the artery increases (right section, arrow) rendering their contours unsharp.

as ringlike structures when imaged "end-on" ("down the barrel"). The normal bronchial wall is about 1 mm thick and barely perceptible. If its thickness increases and its contours become unsharp, this is called "bronchial cuffing" (Fig. 6.35).

f You can recognize a bronchus by searching for the accom-i panying artery: The combination of the two structures looks like an "8" with one ring of it filled.

JJJa, The First Descriptor of Pulmonary Lines

^^ Peter James Kerley was an Irish radiologist who tL A trained in Vienna during the Golden Twenties p j^,_^ of the last century. He later worked in London at the Westminster Hospital. The Royal College of Radiologists named a lecture in his honor. He is said to have been a witty fellow with a flair for extravagant diagnoses. As a normal human being, you should try for the former and avoid the latter.

Viral pneumonia: The interlobular septae can also become engorged in some viral pneumonias, for example, in CMV pneumonia (Fig. 6.37). Again, you see the infamous Kerley lines. Of course, the pulmonary venous redistribution typical of pulmonary venous congestion is usually absent and the clinical presentation is quite different from pulmonary edema.

Miliary tuberculosis: Acute widespread small nodules in the lungs of a patient with clinical signs of an infection point to a miliary tuberculosis (Fig. 6.38a) but can also be caused by a variety of endemic fungal infections such as histoplasmosis, coccidioidomycosis, and blastomycosis, depending a little on which part of the world you work in. If this disease is overcome, the little granulomas tend to calcify (Fig. 6.38b).

• Diagnosis: Paul finds enough signs of pulmonary congestion on the CXR and is convinced that the symptoms are so straightforward that he does not hesitate to diagnose cardiogenic interstitial lung edema. The follow-up CXR supports his interpretation because it shows the progression into typical alveolar edema (Fig. 6.39). The registrars have by now been able to confirm their suspicion of a myocardial infarction with ECG and laboratory findings and have initiated the appropriate therapy. They are still puzzled, however, about the "breathing out of the car window" bit of the history. Paul has already discussed the issue with Joey and both have the same explanation: Being driven at high speed, Mr. Shortbreath breathed against the airstream and thus simulated a PEEP (positive end expiratory pressure) respiration, which serves to keep the terminal airways open. That helped him a lot. (Go ahead and try it out on your way home—but make sure your seatbelt is fastened, stay clear of other cars, and dodge insect swarms!)

I Viral Pneumonia

I Viral Pneumonia

Cytomegalovirus Cxr
Fig. 6.37 This is a section of the CXR of a patient with a cytomegalovirus (CMV)-induced pneumonia; the interlobular septae are thickened. This patient was immunosuppressed after organ transplantation.

f If you ask different people "Does this patient's CXR show i pulmonary edema?" you frequently get different answers—the decision is not always that simple. Try to use the above-mentioned criteria and listen closely to the clinical impression of the registrars in charge of the patient. After a little while you and your perception will be adequately tuned to diagnose this condition with some certainty.

I Miliary Tuberculosis a Active b Inactive a Active b Inactive

Cxr With Congestion
Fig. 6.38a This immunosuppressed HIV patient developed an active miliary tuberculosis. b The tiny, very dense nodules on this radiograph are typical for an inactivated miliary tuberculosis (milium= millet or sorghum). This patient had been admitted for a replacement of his total hip arthroplasty.

I The Case of David Shortbreath

Pulmonary Venous Congestion
Fig. 6.39 This is the follow-up study of Mr. Shortbreath—a portable radiograph that shows an increase in pulmonary venous congestion. In the perihilar region the exudation of fluid into the alveoli is documented by spotty and/or cloudy opacities. The heart is significantly enlarged.

Acute Diffuse Acinar, Confluent (Alveolar) Pattern

Checklist:

Acute Diffuse Alveolar Pattern

Is the consolidation predominantly central or peripheral? Do the vessels appear unsharp or cranially distended? Are the perceptible bronchial walls thickened? Is the heart enlarged?

Are there symptoms of a myocardial infarction? Could the fluid balance be positive (patient on hemo-dialysis, intensive care setting, infusion therapy)? Are there signs of infection?

Could an allergic or toxic reaction be present (organic dusts, gas, drugs)?

Something is Filling Up

Mary Chang (57) has been brought to the emergency room straight from her apartment in Bondi. Her neighbor called the ambulance after having found her wheezing at her front door. Currently Mrs. Chang cannot be questioned because the ambulance medics had to sedate and intubate the distressed patient. Giufeng tries to get some information from the friendly neighbor who accompanied her to the hospital: Yes, she overheard a loud argument and the slamming of doors in Mrs. Chang's apartment quite a while before she found her. But she is not really close to her next-door neighbor. Giufeng is a little perplexed as she returns to her viewbox where the CXR and Hannah are already waiting for her (Fig. 6.40). Hannah has spotted a policewoman together with a detective in the emergency waiting area.

^ What Is Your Diagnosis?

Pulmonary edema: A lung edema due to an increase in the pressure of the pulmonary circulation could certainly be present (see Fig. 6.36b, Fig. 6.39). This could be due to a myocardial infarction, which must be excluded in this case. A patient with renal insufficiency in dire need of a dialysis could also present with an image like that.

Pulmonary hemorrhage: In pulmonary hemorrhage, as may occur in Wegener granulomatosis or in Goodpasture syndrome, the alveoli fill with blood (Fig. 6.41).

Hypersensitivity pneumonitis due to exogenous allergens: The inhalation of many different allergenic organic substances such as bird excrement, the dust of bird feathers, moldy hay or barley, paper or sawdust can initiate a massive pulmonary hypersensitivity reaction including exudation of fluid into the alveoli.

Pneumocystis carinii pneumonia: In an AIDS patient with the symptoms of a pulmonary infection, Pneumocystis carinii pneumonia is very probable (Fig. 6.42).

I The Case of Mary Chang

Dust Pneumonia
Fig. 6.40 Observe the CXR of Mrs. Chang. Which diagnoses must be discussed?

I Lung Hemorrhage

Fig. 6.41 This elderly lady had a heart valve implanted. Postoperatively a fulminant pulmonary hemorrhage resulted that led to this remarkably dense opacification (hemosiderin content!) of both lungs.

Fig. 6.41 This elderly lady had a heart valve implanted. Postoperatively a fulminant pulmonary hemorrhage resulted that led to this remarkably dense opacification (hemosiderin content!) of both lungs.

I Pneumocystis carinii Pneumonia

Pneumocystis Carinii
Fig. 6.42 A severe Pneumocystis carinii pneumonia occurred in this HIV patient. Changes are much more subtle in most other patients. In these less obvious cases a high-resolution CT (HRCT) is recommended.

Acute respiratory distress syndrome (ARDS): Finally, this could be acute ARDS. While in normal edema intact tissue barriers are crossed because the pulmonary venous pressure is increased, an injury of the barriers with an ensuing increase in permeability may lead to fluid leakage into the alveoli without a pressure hike in the pulmonary circulation. The result is the so-called ARDS (Fig. 6.43a), also called shock lung or (formerly) "DaNang lung." The increase in permeability may be due to a variety of causes. However, severe hypoxemia always develops and must be compensated by ventilating the affected patient with a high oxygen concentration gas mixture. As the patients are being ventilated with high pressures, pneumothoraces are always a danger and must be excluded (Fig. 6.43b). In a

I Acute Respiratory Distress Syndrome (ARDS)

Alveoli Con Membrane Ialine Ards

Fig. 6.43 a Subsequent to a pneumonia this patient developed a serious disturbance of pulmonary membrane permeability compatible with ARDS. b Patients with ARDS often have to remain on the respirator for prolonged periods and are frequently ventilated with high end-expiratory pressures. Pneumothoraces requiring pleural drainage are a possible complication. In this patient several pleural drains have already been introduced on both sides. The left lung is still not completely expanded.

Fig. 6.43 a Subsequent to a pneumonia this patient developed a serious disturbance of pulmonary membrane permeability compatible with ARDS. b Patients with ARDS often have to remain on the respirator for prolonged periods and are frequently ventilated with high end-expiratory pressures. Pneumothoraces requiring pleural drainage are a possible complication. In this patient several pleural drains have already been introduced on both sides. The left lung is still not completely expanded.

Danang 1961

few cases a special dedicated technique may help: instead of with air, the patients are respirated with a special fluid that permits extremely good gas exchange and at the same time soothes the pulmonary membranes (Fig. 6.43c).

Why Was This Disease Called "DaNang Lung"?

DaNang is a city in Indochina that became infamous during the Vietnam war (1961-1975). Your parents and grandparents remember the depressing stories in the daily news: helicopters flew wounded soldiers back from the jungle to the modern American military hospital in DaNang. It was there that heavily traumatized soldiers with high blood losses could be transfused with blood and plasma. In these patients a hitherto unknown form of pulmonary edema was observed that developed after the successful therapy of their shock. Prolonged artificial respiration with high oxygen pressures was necessary to treat this disease—ARDS.

Miscellaneous severe alveolar reaction: The acute flooding of the lung with particles, such as may happen in sand blasting without breathing protection, can lead to an extensive alveolar disease pattern. The same is true in massive aspiration of fluids (as in drowning) and the inhalation of toxic gases.

• Diagnosis: Giufeng and Hannah are a little frazzled. Gregory, who has dropped by, also does not have a good explanation, lacking any clinical background information on this patient. The heart is in good shape the cardiologist states having looked at the ECG and the laboratory parameters. Pulmonary hemorrhage has been excluded during bronchoscopy. An HIV infection is improbable. Fortunately, under artificial respiration and cor-ticosteroid therapy, Mrs. Chang's health improves quickly. A few days later, after extubation and further recovery, she tells her story. After her ex-husband's short visit, she had cleaned the guest toilet with her very own cocktail of strong toilet cleaners. While polishing the toilet seat in this small room she suddenly began to feel very short of breath, gasped for air, and almost collapsed. It was most likely a case of acute toxic lung edema. Her ex-husband was involved only tangentially, having recklessly or deliberately peed on the toilet seat for old times' sake.

The lungs can only react in a limited number of ways to external injury. At the beginning of the evaluation it is important to determine the most likely offending agent, often through pertinent clinical history provided by the patient or witnesses. If specific information is unavailable, the problem is classified according to the symptomatology, prevalence of the disease, and plausibility.

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Responses

  • gabriel
    What is upper lobe venous congestion?
    5 years ago
  • Adalberta Conti
    What is pneumocystis carinii pneumonia?
    3 years ago

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