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
Identify the Abnormality (click for a hint)
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
Identify the Abnormality (click for a hint)
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
Identify the Abnormality (click for a hint)
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
Identify the Abnormality
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
Identify the Abnormality
Enlarged cardiac silhouette
“Superior pericardialborder” sign
Hint…patient iss/p CABG surgery
Pericardial Effusion
Pericardial Effusion – Lateral View
Enlarged cardiac silhouette
“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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