ICU Radiography Diseases that Develop Within 24 hrs and Longer in Critical Care Patients Tyler Andrews OHSU-MS4 September 20, 2004 Skeena River, BC
Aspiration: OFTEN to blame for fever
Atelectasis: NOT to blame for fever
Pulmonary Edema: hydrostatic vs. capillary leak vs. diffuse alveolar damage
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
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 performed to remove mucous plug Elevated, convex minor fissure
Refers to collapse or loss of lung volume
Results from a number of causes:
Obstructive – mucous plugging, inflammatory debris, foreign body
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-glass opacification of LLL Atelectasis (non-obstructive)
Atelectasis Versus Aspiration Both demonstrate dependent, ground-glass opacities with air-bronchograms … however Atelectatic air- bronchograms are often compacted together … while aspiration air-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
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!
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.
Infectious Pneumonia: >24 Hours
> 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!
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
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, patchy areas 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 distribution of 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
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 of vascular markings Little or no mediastinal shift noted Pneumothorax (simple)
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 shifted to contralateral side Conversion to Tension Pneumothorax
Same patient…proper valve placement
Simple or Tension Pneumothorax? Neither Skin fold Take 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? Pneumothorax Skin fold Note the opaque edge of the visceral pleura Line vs. Stripe interface Vs. the stripe pattern seen with skin folds
Identify the Abnormality Enlarged cardiac silhouette “ Superior pericardial border” sign Hint…patient is s/p CABG surgery Pericardial Effusion