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ICU Radiography

ICU Radiography






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    ICU Radiography ICU Radiography Presentation Transcript

    • ICU Radiography Diseases 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 performed to remove mucous plug Elevated, convex minor 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-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
        • 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, 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
        • 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 of vascular markings Little or no mediastinal shift 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 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
    • 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 (2 nd Edition). Lippincott Williams and Wilkins 1999.
      N. Umpqua River, OR