Pleura

Read first the text book: Computed Tomography and Magnetic resonance of the Thorax by Nadich et all

Then go through this exercise to assess your comprehension

Q1: What are the issues we have to decide in evaluating pleura?

Anatomy

Serous Membrane

Visceral and parietal division, approximately equal surface area. Each is 1 layer of mesothelial cells, basement membrane,
connective tissue, microvessels and lymphatics

Mesothelial Cells
Single layer, pleomorphic. Surface microvilli, more dense on visceral side of pleura

Stomata
Opening between cells, 2-12 um, only on the parietal surface. The usual exits into lymphatic lacunae for liquid, protein,
and cells

Blood Supply
Some controversy. Human visceral pleura supplied by systemic bronchial vessels, drain through fairly large capillaries
to pulmonary veins. Parietal blood from adjacent chest wall, drainage to bronchial veins; diaphragmatic pleura supply
from nearby arteries, drainage to inferior vena cava and brachiocephalic trunk

Lymphatics
More dense lower and toward the mediastinum. Drainage toward hilum either via lung or pleura itself. Stomata lead to
lacunae which form valves. Drain to mediastinum via intercostal route depending on origin. Visceral pleural drainage to
middle mediastinal nodes or posterior (lower lobes)
True Concepts

Fluid formed at parietal surface - Pressure gradient from parietal pleural intestinum to pleural space due to
subatmospheric pleural space pressure. Little from visceral surface.
Pleural protein filtered to 0.3-9.4 g/dl, then water reabsorbed leaving 1-1.5 g/dl
Lower filtration rate found with radiolabeled albumin studies in sheep by Staub, et al. Old data, likely due to
model (dog) and inflammation from pleural catheters. Lymphatics with large reserve - if fluid accumulates, there is
both increased fluid formation and decreased clearance

Six mechanisms of pleural fluid accumulation

Increased hydrostatic pressure, especially systemic venous pressure combined with capillary wedge pressure in CHF
Decreased oncotic pressure - by itself not a huge problem because of lymphatic reserves
Decreased (more negative) pleural pressure - collapsed or trapped lung
Increased permeability of microvasculature, inflammatory fluid formation
Impaired lymphatic drainage - blockage of channels with tumor, fibrosis, etc.
Fluid from peritoneal space - ascites moves via diaphragmatic lymphatics or diaphragmatic defects (less
than 1 cm)
Gas absorption - dependent on N2 gradient. In pneumothorax, 02 therapy increases gradient of N2 from pleural
space to venous blood

Pleural Fluid Analysis (Diagnostic Tests)

Thoracentesis

Indications: effusion without a secure clinical diagnosis (e.g., CHF) or small quantity

Contraindications: none absolute, relative risk > benefit, bleeding diathesis, small effusion, mechanical ventilation, anticoagulation

Complications:

Subjective: anxiety, site pain

Objective: pneumothorax (12% at a University H), 1/3-1/2 of those require check tubes; fluid contaminated with blood, "dry tap"; empyema; puncture of other organs (e.g., liver); hypoxemia and unilateral pulmonary edema only with therapeutic taps - usually large and occur with carcinoma or trapped lung

Benefit: relief of dyspnea with therapeutic tape - via reduction of chest wall size even though hypoxemia occurs

Diagnostic yield:

Almost 75% of thoracentesis yield a specific or presumptive diagnosis; 15-20% more are useful in management (e.g., rule out empyema)

Specific diagnoses: malignancy (cells), empyema (pus), tuberculosis pleurisy (AFB), fungal infection (KOH), lupus pleuritis (LE cells), chylothorax, urinothorax fluid creatinine/serum creatinine greater than 1), esophageal rupture (high fluid amylase, Ph about 6.0)
Tests that should be run (35-50 ml fluid): LDH, protein, WBC count and differential, glucose, Ph; concomitant serum protein, LDH, glucose; arterial pH if fluid pH <7.30 and acidemia is suspected.

Supplement with other reasonably requested analyses cytology, cultures, smears, immunology, amylase,
lipids, CEA, etc.

Results:
Exudate vs. transudate:
(1) Fluid/serum protein ratio > 0.5
(2) Fluid/serum LDH ration > 0.6
(3) Fluid LDH > 2/3 upper normal serum LDH; exudates have 1 or more; transudates none these
characteristics
If LDH only is abnormal - consider malignancy or parapneumonic effusion
Protein may confuse: e.g., CHF <3 g/dl, but might be 3-4 g/dl if patient uses diuretics, or is chronic or
recurrent
WBC: rarely diagnostic alone; > 50,000 in parapneumonic effusion, usually empyema; > 10,000 very inflammatory

(1) Early, acute, PMN predominant

(2) Later mononuclear - high counts suggest TB, carcinoma, lymphoma, sarcoidosis

(3) Eosinophilia - 10% suggest benign, self- limited; commonly with air or blood in pleural space; consider: hemothorax, pulmonary infarction, pneumothorax, previous thoracentesis, parasitic diseases, fungi, drugs, asbestos; rare with TB or malignancy. In 1/3 "idiopathic"

(4) Basophilia - 10%, rare; suggest leukemia

Mesothelial cells - paucity of cells occurs with chronic diffuse pleural lesions, e.g., TB, malignancy, empyema rheumatoid effusion, pleurodesis. If > 5%, essentially rules out TB
Bloody (> 100,000 cells/mm3): malignancy, trauma, pulmonary embolism, post-cardiac injury, asbestos pleurisy
Cytology: yields nearly 90% with malignancy as cause

Percutaneous Pleural Biopsy

Indication: undiagnosed exudate, especially lymphocytic (yield: TB - 75%, over 90% with AFB culture of tissue; malignant 60%)
Contraindications: obliterated pleural space, anticoagulation, uncooperative patient, bleeding diathesis
Complications: similar to thoracentesis

Thoracoscopy

Indications: controversial because it usually requires hospitalization, and only increased yield a small amount.
Pleurodesis can be done at the same time
Contraindications: like closed biopsy
Complications: tumor seeding common

Open Biopsy

With thoracotomy and autopsy, the "gold" standard - but risk and cost are relatively high
Specific Diagnoses

Transudates

CHF, cirrhosis, peritoneal dialysis, urinothorax, nephrotic syndrome, atelectasis

Selected Exudates (There are many other causes besides these )

Parapneumonic - uncomplicated: LDH <700, glucose="serum," pH> 7.30
Parapneumonic - complicated: LDH > 1000, glucose <40, pH < 7.10
TB - lymphocytic exudate; pleural biopsy is diagnostic
Carcinoma - bloody, lymphocytic exudate, cytology or biopsy positive; if LDH only is abnormal - think cancer;
pH <7.30 associated with poor prognosis and poor response to sclerotherapy
Esophageal perforation - pH 6.00, high amylase (salivary)
Rheumatoid pleurisy - turbid, yellow-green, debris- laden fluid; LDH > 1000, glucose <30, pH 7.00, RF> 1:320
Lupus - LE cells in effusion (increase if fluid sits up to 24 hours): occasionally low glucose and pH
Post-cardiac injury syndrome - pleuritic pain, rub, fever 3 weeks after injury; left infiltrates, serosanguineous - no
diagnostic labs
Pulmonary embolism - nothing characteristic; fluid maximal by 72 hours
Pancreatitis - usually left sided, pleural fluid amylase: serum amylase > 1.0; amylase may be > 100,000 with
pseudocyst
Asbestos pleural effusion - asymptomatic; bloody exudate, unilateral
Trapped lung - unilateral; serous, "borderline" exudate, very low pleural liquid pressure, rapid reaccumulation
Chylothorax - lymphocytic, milky; chylomicrons in fluid, TG > 110 mg/dl
Lymphangiomyomatosis - chylothorax in a young women, interstitial disease, normal lung volumes, repeated
pneumothoraces
Yellow nail syndrome - 40 years old with yellow nails, lymphedema, respiratory tract involvement, triad not
simultaneous; pleurodesis effective
The pleural cavities are closed sacs enveloping each lung. Each cavity comprises a visceral layer
(green) and a parietal layer (blue). The visceral layer is closely apposed to the lungs and cannot
be dissected from the surface. The parietal layer is thicker and is attached to the walls of the
thorax (e.g., diaphragm, ribs, etc). The layers are continuous at the hilum of the lung.

It is important to understand the reflections of the parietal and visceral pleura on the thoracic wall as seen from anterior, lateral, and side. Generally, the visceral pleura (lungs) are 2 ribs more superior than the parietal pleura at mid inspiration.

Anteriorly

(1) the pleura reach the midline at rib 2
(2) the pleura deviate to the left at rib 4 (cardiac notch)
(3) the pleura deviate to the right at rib 6
(4) the visceral pleura reaches rib 6 at the mid-clavicular line (vertical bar)
(4) the parietal pleura reaches rib 8 at the mid-clavicular line (arrow)
Laterally the visceral pleura reaches rib 8 at the mid-axillary line (vertical bar) the parietal pleura reaches rib 10 at the mid-axillaryr line

Posteriorly the visceral pleura reaches rib 10 the parietal pleura reaches rib 12

The pleural cavities are closed sacs enveloping each lung. Each cavity (grey area) comprises a visceral layer (green) and a parietal layer (blue). The visceral layer is closely apposed to the lungs and cannot be dissected from the surface. The parietal layer is thicker and is attached to the walls of the thorax (e.g., diaphragm, ribs, etc). The layers are continuous at the hilum of the lung.

Drawing of the pleural cavity showing the right lung (dark green) lined by visceral pleura (1) and parietal pleura (2) between which is the pleural sac (3).

A. Parietal pleura - this is the outer layer which is divided into:

1.costal pleura - lines the ribs
2.diaphragmatic pleura - lines the diaphragm
3.mediastinal pleura - lines the mediastinum

B. Visceral pleura - this layer covers the lungs.

C. Pleural recesses -recesses are formed between the parietal and visceral pleura forming potential spaces allowing maximum expansion of the lung during forced ventilation. Two which you should know are:

1.costodiaphragmatic recess

2.costomediastinal recess.

B. Pleural reflections onto the thoracic wall. Drawing of the pleural cavity showing the costodiaphragmatic recess (arrow). This is only a
potential space into which the lung can expand on deep inhalation.

Anatomical and Physiologic Principles

The lower limit of pleura is 10th interspace posteriorly and 6th anteriorly. Hence gravity facilitates accumulation of fluid in the gutter posteriorly first. With most etiologies (except negative pressure induced pleural effusion) once the fluid accumulates in pleural space the negative pressure decreases and eventually becomes positive. Loss of negative pressure in pleural space results in higher resting position of hemithorax. The lung relaxes and becomes smaller since there is no negative pressure to hold it close to chest wall.
Once the pressure becomes positive the mediastinum and diaphragm get pushed. The diaphragm eventually can become concave upwards.
Fluid is subpulmonic to start with the lung relaxes and floats attached to hilum. As the lung retracts towards hilum, fluid tracks up between visceral and parietal pleura. Fluid has a broad base and thin apex along the chest circumference. The meniscus appearance of
the fluid is a visual illusion, thickness of fluid level is higher along sides compared to the middle.
Fluid moves freely and shifts with position. As the pleural pressure increases with more fluid formation i.e. massive pleural effusion
the lung becomes completely atelectatic. Airways are patent. Fluid is a good conductor of sound.

Q1: What are the issues we have to decide in evaluating pleura?

Confirming presence of lesion
Precise location and extent Pulmonary parenchymal or pleural
Nature of pathology by means of attenuation coefficients

Q2: When a lesion is found in the periphery, what are the possible sites where the lesion can be located?