7.5 Pleura Flashcards
Describe the anatomy of the pleura.
Pleurae refer to the serous membranes covering the lung, mediastinum,
diaphragm, and the inside of the chest wall.
Two layers, visceral and parietal membranes, meet at the lung hilum.
- Visceral:
attached closely and adheres to the whole surface of the lung,
enveloping the interlobar fissures. - Parietal:
the outer layer, which is attached to the chest wall and the
diaphragm and named as mediastinal, diaphragmatic, costal and cervical
pleura, as per the association with the adjacent structures.
The potential space between the two layers is called pleural space and is
filled with a small amount of fluid amounting to around 0.2 mL/kg (5–10 mL).
This is determined by the net result of opposing Starling’s hydrostatic and
oncotic forces and lymphatic drainage.
Pleural fluid as little as 1 mL serves as a lubricant and decreases friction between the pleurae during respiration.
What are the constituents of pleural fluid?
- Clear ultrafiltrate of plasma
- Quantity: 0.2 mL/kg (8.4+/– 4.3 mL)
- Cellular contents: 75% macrophages, 25% lymphocytes
- Biochemistry:
Compared to plasma,
the pleural fluid is alkaline (pH @ 7.6)
and has higher albumin content but
lower sodium,
chloride,
and LDH contents.
What is the blood supply of pleura?
- Visceral pleura is supplied by the bronchial arteries and drains into the
pulmonary veins. - Parietal pleura gets its supply from systemic capillaries
including:
intercostal,
pericardiophrenic,
musculophrenic,
internal mammary
Venous drainage is via the
intercostal veins
azygos veins,
finally draining into the
SVC and IVC.
How is pleura innervated?
The visceral pleura do not have pain fibres
is supplied by the
pulmonary branch of vagus nerve
+
the sympathetic trunk.
The parietal pleura receives
extensive innervation:
somatic intercostal
+
phrenic nerves.
Explain the starling’s forces and describe the pathogenesis of pleural effusion.
The movement of pleural fluid
between the pleural capillaries and the
pleural space is governed by
Starling’s law of transcapillary exchange.
Net filtration = Kf [(Pc − Pi) − σ(πc − πi)]
What do the elements of Net filtration equation mean
Net filtration = Kf [(Pc − Pi) − σ(πc − πi)]
Kf: filtration coefficient and is dependent on the area of the capillary walls and
the permeability to water..
σ: reflection coefficient and is the ability of the membrane to restrict passage
of proteins.
Pc and Pi: Hydrostatic pressure in capillary and interstitium respectively.
πc and πi: osmotic pressure in capillary and interstitium respectively.
Pathogenesis of pleural effusion
- increased formation
- Decreased reabsorption
increased formation
- Increased interstitial fluid in the lung: LVF, PE, ARDS
- Increased pressure in capillaries: LVF/RVF, SVC syndrome, pericardial
effusion - Increased interstitial pressure: para pneumonic effusion
- Decreased pleural pressure: lung atelectasis
- Increased fluid in peritoneal cavity: ascites, peritoneal dialysis
Decreased reabsorption
- Obstruction of lymphatics: pleural malignancy
- Increased systemic vascular pressures: SVC syndrome and RVF
How to differentiate an exudate from transudate
Light’s criteria differentiates an exudate from transudate.
The pleural fluid is an exudate if one or more of the following criteria are met:
- Pleural fluid: serum protein > 0.5
- Pleural fluid: serum LDH > 0.6
- Pleural fluid LDH more than two-thirds the upper limits of normal serum LDH
Exudates
Due to local pleural and pulmonary disease
Causes
* Malignancy
* Parapneumonic effusions
* Pulmonary infarction
* Rheumatoid arthritis
* Autoimmune diseases
* Pancreatitis
* Postmyocardial infarction syndrome
Transudates
Due to systemic factors that influence the formation and reabsorption of pleural fluid
Causes
* Left ventricular failure
* Liver cirrhosis
* Hypoalbuminaemia
* Peritoneal dialysis
* Nephrotic syndrome
* Mitral stenosis
* Pulmonary embolism
What drugs are known to cause pleural effusions?
- Amiodarone
- Phenytoin
- Methotrexate
- Carbamazepine
- Propylthiouracil
- Penicillamine
- Cyclophosphamide
- Bromocriptine
What are the effects of pneumothorax on pleural pressure?
Basic concepts
- At FRC, due to the tendency of the lung to collapse and the chest wall
to expand, the pleural pressure is maintained negative.
This negative pressure holds the alveoli open.
- Also due to gravity, the pleural pressure at the base
of the lung is higher than that at the apex (more negative at the apex).
If chest wall is pierced (open pneumothorax)
or the visceral pleura is breached (closed pneumothorax),
air leaks into the pleural cavity causing a pneumothorax
until the pressure gradient no longer exists.
Because the thoracic cavity is below its resting volume
and lung above its resting volume,
with a pneumothorax,
the thoracic cavity enlarges and the lung becomes
smaller and hence collapses.
The pleural pressure is same throughout the entire pleural space,
as per point (2), with the upper lobe being more affected than the lower lobe.
In tension pneumothorax, air enters into the pleural cavity with inspiration
but cannot leave due to a flap of tissue acting as a one-way valve.
The developed pressure collapses the affected lung
if high enough can cause a mediastinal shift.
What are the indications of intercostal drain in pneumothorax and pleural effusions?
Pneumothorax
* In any ventilated patient
* Tension pneumothorax after initial decompression
* Persistent or recurrent pneumothorax
Pleural effusion
* Large and symptomatic effusion
- Malignant pleural effusion, chylothorax
- Traumatic haemo pneumothorax
- Empyema
- Postoperative, for example,
thoracotomy, oesophagectomy, cardiac surgery
