ICU Radiography

ICU RadiographyDiseases that Develop Within 24 hrs and Longer in Critical Care Patients

Tyler Andrews OHSU-MS4 September 20, 2004

Skeena River, BC

Major Considerations

• Aspiration: OFTEN to blame for fever

• Atelectasis: NOT to blame for fever

• Pulmonary Edema: hydrostatic vs. capillary leak vs. diffuse alveolar damage

• Infectious Pnuemonia

• Pneumothorax

• Pericardial Effusion

Identify the Abnormality (click for a hint)

Air Bronchogram

ETT

Ill-defined, focal consolidation (not “prominent vasculature”)”)

…12 hours later

Progression to ill-defined, patchy consolidation < 24 hrs

Aspiration

Aspiration Pneumonitis

• There are usually two requirements to produce aspiration pneumonitis:– Compromise in the usual defenses that protect the lower airway

including glottic closure, cough reflex, and other clearing mechanisms

– An inoculum deleterious to the lower airways by a direct toxic effect, stimulation of inflammatory response, or obstruction

• Predisposing conditions seen in the ICU:– Reduced consciousness/altered mental status

– GERD, upper airway/esophageal surgery

– Protracted vomiting, nasogastric feeding, recumbent position

– Mechanical disruption of the glottic closure

• Tracheostomies, endotracheal tubes, bronchoscopy

• …But don’t ETTs protect the airway?– No! – Patients still aspirate 24/7

– Aspiration is a common event even in healthy individuals and usually resolves w/o detectable sequelae

• Clinical features that should raise suspicion– Abrupt onset of symptoms, prominent dyspnea

– Fever, usually low-grade

– Cyanosis and diffuse crackles upon auscultation

– Severe hypoxemia despite oxygen supplimentation

• Quick onset Quick resolution– Radiographic changes can often be noted within two

hours of the aspiration event

Did this Patient Aspirate?

Absolutely!

Foreign body (tooth) aspirated into R. mainstem

bronchus during laryngoscopy


RUL Collapse

Lack of air bronchograms

Atelectasis (post obstructive)

Bronchoscopy should be performedto remove mucous plug

Elevated, convexminor fissure

Atelectasis

• Refers to collapse or loss of lung volume• Results from a number of causes:

– Obstructive – mucous plugging, inflammatory debris, foreign body

– Nonobstructive– Compressive – pleural effusions

– Adhesive – lack of surfactant (ARDS/DAD)

– Cicitrization – radiation, necrotizing pneumonia

– Relaxation – pleural effusion, pneumothorax

– Replacement – alveoli of an entire lobe are replaced by tumor

Do You Perform a Thoracentesis?

No…This is obstructive ateletasis secondary to mucous plugging

Pleural effusion would shift the trachea to the R.

Would bronchoscopy help in this patient?

No…airways are patent

Tightly “packed” air-bronchograms

Diffuse, ground-glassopacification of LLL

Atelectasis (non-obstructive)

Atelectasis Versus Aspiration

Both demonstrate dependent, ground-glass opacities with air-bronchograms

…however

Atelectatic air-bronchograms

are oftencompacted

together…while aspirationair-bronchograms

are often more wide-spread

Does Atelectasis Cause Fever?

• Postoperative fever occurs in many patients– Causes include infection, hematoma, pulmonary

embolism, malignant hyperthermia, and drug fever however… often times atelectasis, if present, may be blamed

• Engoren et al. – Studied 100 consecutive postoperative cardiac surgery

patients admitted to the ICU through the second postoperative day with portable CXR’s and continuous bladder thermometry

– Radiographs were read by the same, blinded observer– Results:

• daily incidence of atelectasis increased from 43 69 79%• However, incidence of fever (temp > 38.0 degrees C) fell from

37 21 17%

• Lansing et al.– 1963 - Made early attempts at elucidating a

mechanism of how atelectasis caused fever• Cotton plugs (non-sterile) were placed in the left-

main bronchus of 30 dogs. Animals became febrile within 12 hours. Distal to the plug, the bronchial tree was found to be “filled with a thick mucopurulent exudate.”

• 6 animals were treated with penicillin/streptomycin at the time of bronchial plugging. “Only very slight rises in temperature” were seen in these animals.

• Authors concluded that fever, but not atelectasis was prevented by antibiotics…why?

• Atelectasis was not responsible for the fever it was post-obstructive pneumonia!

• Bottom Line– Atelectasis does not cause fever, if anything, it

is inversely correlated with fever.– While atelectasis may cause pulmonary

shunting and hypoxemia and require treatment for these reasons, attributing fever to atelectasis may lead to missing infection or to inappropriate therapy.

– Look elsewhere!

Infectious Pneumonia: >24 Hours

Infectious Pneumonia• > 20% of nosocomial infections are acquired in

ICUs• Ventilator Associated Pneumonia (VAP)

– Infection of lung tissue that develops 48 hours or more after intubation in mechanically ventilated patients.

– Mechanical ventilation increases the risk of developing pneumonia 7 to 21% ETTs are not protective!

– Risk factors• Age > 60, chronic lung disease (COPD), ARDS, duration of

ventilation, aspiration, paralytics, nasogastric tube, delay in extubation of patients who meet criteria

– Radiographically similar to aspiration or atelectasis• The key is the duration to onset > 24 hours

Pulmonary Edema

• Divided into two major forms– Hydrostatic Edema (CHF) – develops and

resolves quickly, often with no radiologic lag. In fact, radiologic findings often precede clinical symptoms

– Capillary Leak Edema (ARDS) – Also develops quickly, but tends to resolve much slower due to alveolar epithelial damage

• These forms do not look alike and often can be distinguished on the chest radiograph


Dependent, ground-glass opacities bilaterally

Vascular indistinctness

Enlarged cardiac silhouette

Hydrostatic Edema (CHF)

Cardiogenic (Hydrostatic) Edema

• Results from increased pressure in pulmonary capillaries left ventricular failure, volume overload, etc.

• Edema can manifest as indistinctness of vessels, subpleural thickening along interlobar fissures, peribronchial cuffing, and septal (Kerley A/B) lines.

• If hydrostatic edema is severe enough to flood the alveoli, it usually has a central or basilar distribution.

• Duration of edema also affects distribution– Initially, edema is distributed evenly eventually it may clear

peripherally but persist centrally (~ 1 week)

– Redistribution (cephalization) only occurs in the setting of chronic pulmonary venous hypertension (mitral stenosis, etc.)

Hydrostatic Edema – CHF(comparison film is your best friend)

…Again, note vascular indistinctness

Soft tissue edema

Wide vascular pedicle(volume overload)

…Hydrostatic Edema Continued

Lateral projection is best for detection of…?

Kerley-A’s

Kerley-B’s


Diffuse, patchyareas of consolidation

…with sparing of the lower lobes

SGC reads 20 mmHG…do you believe it?

“Aztec sign of death”(defibrillator pad)

35% false positive rate

Non-Cardiogenic Edema

Noncardiogenic (Capillary Leak) Edema

• Results from disruption of the capillary endothelium with leakage of plasma into the surrounding lung tissue.

• Much more common than cardiogenic edema• Causes include sepsis, pneumonia, hypotension,

trauma, burns, DIC, pancreatitis, transfusion reactions, air embolism, and toxic inhalation

• Two other pulmonary disorders may be confused with capillary leak edema:– Diffuse alveolar hemorrhage – should be considered in

association with an unexplained drop in hemoglobin concentration

– Cancer dissemination – rarely occurs in the ICU setting

ARDS/Diffuse Alveolar Damage

Same patient…compare lung volumes

Peripheral distributionof opacification

Decreased compliance=

Decreased lung volume

Identify the Abnormality

Hint…this patient will

Require intubation very soon

ARDS/Diffuse Alveolar Damage

• Considered the severest form of capillary leak edema, in which alveolar epithelial injury is the determining factor.

• Pathological findings are divided into 3 stages:– Exudation – edema, hemorrhage, hyaline membranes

– Proliferation – organization

– Fibrosis

• Radiographic findings– Peripheral distribution and lack of effusion favors ARDS

– Serial exams may be helpful ARDS clears very slowly

– Is the patient intubated? with ARDS, even mild lung opacification is almost always associated with severe enough hypoxia to require mechanical ventilation


Visceral Pleura

Absence ofvascular markings

Little or nomediastinalshift noted

Pneumothorax (simple)

Pneumothorax

• Refers to gas in the pleural space and can be divided into several types:– Simple – pleural pressure becomes slightly more

positive, but still remains subatmospheric

– Tension – intrapleural pressure exceeds atmospheric pressure resulting in a “check valve” mechanism, which promotes the inspiratory accumulation of gas. As a result, the diaphragm may be depressed and the mediastinum shifted to the contralateral side.

– Don’t be fooled by skin folds! Beware of the classic stripe pattern and vasculature that extend beyond the alleged pneumothorax.

Same patient…what happened?

“One-way” valve placed backwards

Flattening of R hemidiaphragm

R. visceral pleura,mediastinum shiftedto contralateral side

Conversion to Tension Pneumothorax

Same patient…proper valve placement

Simple or Tension Pneumothorax?

Neither Skin foldTake a closer look

(next slide)

Line vs. stripe interface(see next slide)

Skin Fold

Try to follow vasculature to the periphery

Which patient just bought a chest tube?

PneumothoraxSkin fold

Note the opaque edgeof the visceral pleura

Line vs. Stripe interface

Vs. the stripe patternseen with skin folds



“Superior pericardialborder” sign

Hint…patient iss/p CABG surgery

Pericardial Effusion

Pericardial Effusion – Lateral View


“Oreo” sign

Retrosternal fat

Epicardial fat

Pericardial effusion

Pericardial Effusion

• Should be considered with unexplained new radiographic cardiomegaly without pulmonary congestion, particularly in the ICU setting.

• Risk factors:– Myocardial infarction, cardiac surgery, or an invasive cardiac

diagnostic or interventional procedure

• Contrary to common teaching, pericardial effusion can be diagnosed on history, physical exam and radiography alone echocardiography is not required.

• Radiographic signs:– Increased cardiac silhouette

– “Superior pericardial border” sign

– “Oreo” sign – blood/cardiac fat interface

References• Chastre, J, Fagon, JY. Ventilator-associated Pneumonia. Am J Respir Crit Care Med 2002;

165:867.• Ketai, L, Godwin, J. A New View of Pulmonary Edema and Acute Respiratory Distress

Syndrome. Journal of Thoracic Imaging 1998; 13:147-171.• Engoren, M. Lack of Association Between Atelectasis and Fever. Chest Jan 1995:81-

84.• Daffner, R. Diagnostic Radiology – The Essentials (2nd Edition). Lippincott Williams

and Wilkins 1999.

N. Umpqua River, OR

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ICU Radiography