Monday, September 18, 2017

Interstitial Lung Disease

This post is derived from notes I took during training. Any images are copyright their respective owners.

Interstitial Lung Disease

  • Questions to ask
    • volumes reduced (fibrotic) vs. increased (airways disease)
    • distribution upper (trapped inhaled particulates) vs. lower (blood, lymphatic flow)
    • central vs. peripheral
    • centrilobular vs. septal
  • Interstitial disease
    • All tend to be related to smoking
    • causes peribronchial cuffing, which looks the same as bronchial wall thickening
  • Nonspecific Interstitial Pneumonia (NSIP)
    • Pathophysiology: homogeneous interstitial inflammation, many started as organizing pneumonia. Many etiologies, including connective tissue disease (*except* rheumatoid arthritis (RA))
    • Findings: lower lobe predominance. Subpleural, symmetric distribution of lower lobe patchy ground-glass opacities (GGO) - dominant feature with reticular opacities and limited traction bronchiectasis.


  • Usual Interstitial Pneumonia (UIP)
    • S l o w l y develop dyspnea, also associated with aspiration
    • Pathophysiology: the radiographic finding consistent with clinical syndrome of Idiopathic pulmonary fibrosis (IPF) - see temporal & geographic heterogeneity with fibroblast foci. For connective tissue disease, only RA gives this pattern.
    • Volume loss predominates fibrosis → honeycombing (dilated respiratory bronchioles) is collapse, not fibrosis
    • Findings: lower lobe peripheral honeycombing with spatial/temporal heterogeneity
    • Prognosis: 50% mortality at 3 years; biopsy has high mortality rate
  • Acute Interstitial Pneumonia (AIP; aka Hamman-Rich, ARDS)
    • Diffuse alveolar collapse with areas of sparing (possibly representing areas of arterial thrombosis) causing reduced volumes over rapid course
    • Treatment: Vent on PEEP mode to keep alveoli open
  • Constrictive bronchiolitis (Bronchiolitis obliterans)
    • Cough, dyspnea, malaise. Radiographically occult usually, may show air trapping/mosaic attenuation
    • Causes: diverse inhalational causes (e.g. Iraq lung, popcorn oil, graft-vs-host disease)
    • DI: hyperinflation, discrete nodules, mosaicism
  • Cryptogenic organizing pneumonia (COP)
    • Organization -  histologically, the incorporation of alveolar material into the interstitial wall by fibroblasts, seen in many processes
    • Findings: Peripheral consolidations or nodules along bronchovascular bundles with surrounding halo of consolidation (atoll / reverse halo sign - nonspecific), air bronchograms, and sparing of peripheral lung
    • 80% likely old infections with progressive scarring
  • Smoking related lung disease
    • Respiratory bronchiolitis (RB)
    • Respiratory bronchiolitis - Interstitial Lung Disease (RB-ILD)
      • Macrophages in interstitium causing GGO/nodules in slightly upper > lower lobes
    • Desquamative interstitial pneumonia (DIP)
      • Demographics: age 30-60s, M:F 2:1
      • Pathophysiology: Misleading name because no desquamation of alveolar epithelium present, but rather cells in alveolar space are pigment laden macrophages, thought to represent end-stage of RB-ILD
      • Findings: GGO and alveolar opacities, lower lobe predominant, ground glass
      • Treatment: steroids
  • Scleroderma
    • Progressive systemic sclerosis, esophageal involvement (patulous esophagus) (80%), cardiac involvement (40%),
    • CXR: fibrosis in lower lobes
    • CT: NSIP >> UIP pattern (4:1)
    • Prognosis: associated with increased lung adenocarcinoma
  • Eosinophilic Pneumonia (EP)
    • Can be secondary to unknown causes (Loeffler pneumonia, Acute EP, Chronic EP) versus secondary to known cause (drugs, fungal, parasitic infections)
    • Findings:
      • Simple / Loeffler: Peripheral ground glass opacities with interlobular septal thickening (ie reverse / photographic negative of pulmonary edema, upper lobe predominance. Positive blood eosinophils
      • Acute EP: bilateral GGO and interlobular septal thickening
      • Chronic EP: homogeneous peripheral airspace consolidation (reverse bat-wing pattern). Differential diagnosis: Churg-Strauss
    • Treatment: Steroids (good response)

References:




     

Thursday, September 14, 2017

Thoracic Masses and Malignancies

This post is derived from notes I took during training. Any images are copyright their respective owners.

Neoplasms

  • Solitary pulmonary nodule (SPN)
    • Defined as a lesion < 3 cm, considered benign if stable for 2 years
    • 50% benign, 40% primary lung cancer, 10% metastasis
    • Signs of benignity
      • Fat
      • Doubling time <1 mo="" or="">16 months
      • Calcification
    • PET-CT avid nodules are much more likely to be malignant, although active granulomatous disease can create false positive.  Bronchoalveolar carcinoma (BAC) or carcinoid may create false negative.
  • Hamartoma
    • Gender ratio M:F 2:3, most asymptomatic
    • Benign mass of mesenchymal origin (possibly chromosome 12), containing fat and calcification if degenerating (popcorn pattern)


  • Small cell lung carcinoma
    • 20% of all lung cancer. Central, rapid growth, early metastasis.
    • Associated with Eaton-Lambert syndrome (proximal muscle weakness), paraneoplastic Cushing's syndrome, SIADH
  • Adenocarcinoma in situ (Bronchoalveolar carcinoma)
    • Peripheral
    • FDG poor so not well seen on PET
    • Bronchogenic cancer often spreads to adrenal glands
  • Synchronous cancers - two separate primaries detected within 6 months of each other without metastases
  • Metachronous cancers - two separate primaries diagnosed at separate times without metastases.
  • Lymphangitic carcinomatosis - reticulonodular opacities, septal lines, mediastinal/hilar lymphadenopathy
  • Inflammatory pseudotumor (inflammatory myofibroblastic tumor) - rare, invasive
  • Solitary fibrous tumor of pleura - associated with hypoglycemia and fibrous hypertrophic osteoarthropathy
  • Superior sulcus (Pancoast) tumor - associated with brachial plexopathy, pupillary / Horner's syndrome triad (ptosis (lid dropping), miosis (pupillary constriction), anhidrosis (loss of sweating))
  • Radiation pneumonitis
    • Acute: 1-3 months post treatment, patchy ground glass opacities, lucencies, volume loss
    • Chronic: 6-12 months, consolidation, traction bronchiectasis, volume loss


References:


     

Monday, July 17, 2017

How To Perform A Ductogram / Galactogram

A ductogram is a minimally invasive exam performed by a radiologist for patients with nipple discharge. Also known as a galactogram, a ductogram should be reserved for patients (typically women) with unilateral, spontaneous clear or bloody nipple discharge. That type of discharge is worrisome for malignancy, specifically an intraductal papilloma. 

Indications: 
Women with bilateral nipple discharge should search for central causes first. A common cause would be a pituitary adenoma, which can be assessed with a prolactin level in conjunction with a contrast-enhanced MRI of the brain with sella-specific sequences.

Women with unilateral discharge that is green, yellow, brown or another color most likely have fibrocystic disease, with the discharge representing cystic contents that have been expelled into the ductal system.

Procedure:
Place the patient in a seated position next to the mammography machine. While some texts advocate performing the cannulation supine, the seated position minimizes risk of needle dislodgment when moving the patient.

After cleaning the nipple with an alcohol swap, ask the patient to express the discharge. If they cannot, consider a warm compress or rescheduling the procedure. Once discharge is evident, use a focal light and magnifying glass to attempt to place the needle. A straight or angled 30 gauge needle connected to a 1 cc tuberculin syringe or 3 cc syringe via tubing is utilized. The needle should slide right into the duct if the trajectory is correct. If not, gently re-orient the needle around the clock in 15-30 degree increments. There should not be any resistance or dimpling of the nipple; when the duct is cannulated, the needle will slide right in. This should be relatively painless for the patient.

Once in place, inject 0.3 to 0.5 cc of contrast. Inject S   L   O   W   L   Y, over a minute or more. This is key to preventing extravasation and opacifying the distal ducts.

After injecting, gently affix the needle to skin with Steristrips. Be careful not to affix too forcefully, as this will sidewall the needle. I recommend 1/8th inch strips if available.

Take CC and ML images to document your findings. Once complete, remove the needle and give the patient 2x2 gauze or similar pads to cover the nipple after discharge to capture the contrast that will leak out.

For further details about the procedure and common findings, please see this RadioGraphics article.


References:

       

Friday, July 7, 2017

Infectious Diseases of the Thorax

This post is derived from notes I took during training. Any images are copyright their respective owners.

  • Aspiration causes pneumonitis with lower pH causing worse reaction.
  • The term 'Pneumonia' is reserved for bacterial super infection with positive cultures
  • Tuberculosis (TB)
    • Findings: variable, can see necrotic lymph nodes
    • Rasmussen aneurysm: aneurysm associated with TB cavity, supplied by systemic bronchial arteries. Can cause massive hemoptysis
    • Reactivation can look like tree in bud nodules with +/- cavitation

  • Miliary TB: 1-2 mm nodules throughout lung
  • Mycobacterium avium complex (MAC)
    • Findings:
      • Elderly white females (Lady Windemere syndrome if suppress cough) get upper lobe cavitary
      • Middle aged males smoker/EtOH get Nodular bronchiectatic forms with clustered centrilobular nodules sparing pleura, irregular bronchiectasis with vol loss, predilection for RML and lingula
  • Fungal infections
    • Present with parenchymal necrotizing granulomatous lesions and regional LA. After acute phase, lung lesions may calcify.
    • Histoplasmosis: can cause large calcification in mediastinum (fibrosing mediastinitis)
  • Pulmonary mycetoma
    • Fungal ball, usually immunocompetent patients with fungal elements colonizing a cavity caused by other disease processes
    • Findings: upper lobes. Hemoptysis secondary to fragile bronchial circulation which feeds cavity wall
  • Allergic bronchopulmonary aspergillosis (ABPA)
    • Demographics: associated with asthma, cystic fibrosis
    • Pathology: Type I IgE and Type III hypersensitivity to aspergillus colonizing bronchial lumen causing inflammation, which releases enzymes that break down bronchial walls
    • DI: central bronchiectasis. Excess mucus production → mucoid impaction
  • Invasive aspergillosis
    • Occurs in immunosuppressed patients
    • Can see confluent nodules with surrounding ground glass halo sign (hemorrhage)


  • Pneumocystis carinii pneumonia (PCP)
    • Demographics: associated with HIV/immunosuppressed patients
    • Pathology: Caused by Pneumocystis jiroveci virus
    • Findings: bilateral perihilar reticular/ground-glass opacities, may consolidate after 10 days. Cysts - upper lobe. Can get spontaneous pneumothorax
    • Nuclear Medicine: Gallium positive
    • DDx: Kaposi (Gallium negative)

  • Viral pneumonia
    • DI: Miliary nodules with ground glass opacities


References:

     

Wednesday, July 5, 2017

What Is The Difference Between Epicondyle and Condyle?

This is a quick anatomy stub post on what is the difference between an epicondyle and a condyle?

First, some definitions:

Condyle: a rounded eminence at the end of long bones, often articulating with another bone. The term comes from the Greek for knuckle

Epicondyle: a bony covering that overlies a condyle, most often used in reference to the distal humerus at the level of the elbow

Anatomic relationships of epicondyles to condyles
Source: Wikipedia
At the elbow, the condyle form the trochlea which articulates with the ulna, and the capitulum, which articulates with the radius. As the image above shows, the epicondyles are medial and lateral to the condyles respectively, and do not have articulations.

The lateral epicondyle is often referenced in patients with tennis elbow, or lateral epicondylitis. The syndrome is an overuse injury of the common extensor tendon, first described in lawn tennis players.

The much less common medial epicondylitis, also known as golfer's elbow, is a similar phenomenon affecting the inner aspect of the elbow.

Findings for both entities are best described on MRI. As always, starting with basic anatomy from a text like Netter's Anatomy is very helpful.