Pleura

What it normally does

• Two layers — one stuck to the lung surface (visceral pleura), one lining the inside of the chest wall, mediastinum and diaphragm (parietal pleura) — with only a few millilitres of fluid between them (of the order of 10 mL in each pleural space in an adult). The fluid behaves like water between two glass slides: the layers slide over each other freely but cannot easily be pulled apart.

  the chest wall drags the lung open with it on every breath in — and anything that gets between the two layers breaks that coupling and the lung stops following the chest wall.

• The space is sealed and the pressure inside it is below atmospheric — about −5 cmH₂O at the end of a quiet breath out, falling to about −8 cmH₂O at the end of a normal breath in and to around −30 cmH₂O or lower with a forced maximal inspiration (negative intrapleural pressure). It exists because the lung's elastic recoil pulls inwards while the springy chest wall pulls outwards, and the sealed space between them is held stretched.

  make a hole in either surface — the lung or the chest wall — and air moves in until the pressure rises towards atmospheric, and the lung collapses down onto its own recoil.

• The parietal layer is supplied by ordinary somatic nerves, and the territories differ: the costal pleura by the intercostal nerves (pain felt over the overlying chest wall), the central diaphragmatic and mediastinal pleura by the phrenic nerve (C3–C5, pain referred to the shoulder tip), and the peripheral rim of diaphragmatic pleura by the lower intercostal nerves (the lower six thoracic nerves, roughly T7–T12, pain referred to the lower chest wall and upper abdomen, which can mimic an acute abdomen). The visceral layer has no somatic sensory supply — only autonomic fibres travelling with the pulmonary plexus — and is insensitive to the stimuli that cause pleuritic pain.

  pleuritic pain is sharp and the patient points to it with one finger, irritation of the central diaphragm is felt at the shoulder tip, and disease sitting on the lung surface can grow painlessly until it reaches the parietal layer.

• Fluid filters in continuously from systemic capillaries in the parietal pleura and is drained out through small holes (stomata) into parietal lymphatics, concentrated on the mediastinal and diaphragmatic surfaces. That drainage has substantial reserve — it can be lifted roughly twenty-fold above baseline when pushed.

  an effusion only forms when production overwhelms that reserve, or when the lymphatic drainage itself is blocked.

What goes wrong

• Pneumothorax (air in the pleural space)← from “The space is sealed and the pressure inside it…”

  A hole in the visceral pleura — classically a small subpleural air-filled blister at the lung apex (bleb) rupturing in a tall, thin young smoker — lets air move down its pressure gradient into the space. Intrapleural pressure rises towards atmospheric, so the lung is no longer held out against the chest wall and recoils inwards. That lung is still perfused but poorly ventilated, so some blood passes through unoxygenated (shunt); hypoxic pulmonary vasoconstriction limits this, which is why a small primary pneumothorax often produces breathlessness with near-normal saturations while a large one causes frank hypoxaemia. A secondary spontaneous pneumothorax is the same event in a lung already damaged by emphysema or other chronic lung disease, and it is far less well tolerated because there is no respiratory reserve to spare.

  Hole in visceral pleura → intrapleural pressure rises towards atmospheric → lung recoils. Sudden pleuritic pain, hyper-resonance, absent breath sounds, visible pleural edge with no lung markings beyond. Primary (well lung, often tolerated, increasingly managed conservatively) versus secondary (damaged lung, poorly tolerated, usually needs intervention).

  You would find: Sudden one-sided sharp chest pain and breathlessness. That side moves less, is hyper-resonant to percussion, and has quiet or absent breath sounds. Erect inspiratory chest x-ray shows a thin white visceral pleural line with black, markingless space beyond it (expiratory films are no longer routinely recommended).

• Tension pneumothorax← from “The space is sealed and the pressure inside it…”

  The tear behaves as a one-way valve: air is drawn in with each breath and cannot get out. Pressure in the space does not just equalise with atmosphere — it climbs above it. The rising intrathoracic pressure and mediastinal shift compress and distort the great veins where they enter the chest and reduce the pressure gradient driving venous return. Filling falls, so cardiac output falls, and the patient develops obstructive shock on top of worsening hypoxaemia. The classic sudden cardiovascular collapse is seen fastest in the ventilated or supine trauma patient, where positive pressure pumps the leak; in a spontaneously breathing patient the picture is usually progressive hypoxaemia and respiratory distress first, with hypotension a late and pre-terminal finding.

  One-way valve → positive intrapleural pressure → mediastinal shift → impaired venous return → obstructive shock. Treat before imaging.

  You would find: Severe breathlessness and respiratory distress with a silent, hyper-resonant hemithorax and rising oxygen requirement; hypotension, tachycardia and distended neck veins are late (and neck veins may be flat if the patient is also hypovolaemic), and tracheal deviation away from the side is a late sign. This is a clinical diagnosis — decompress with a needle or finger thoracostomy (in adults, 5th intercostal space just anterior to the mid-axillary line in the 'safe triangle'; the older 2nd space mid-clavicular route often fails to reach the pleura through the adult chest wall) and then place a chest drain. Do not wait for an x-ray in an unstable patient.

• Pleural effusion← from “Fluid filters in continuously from systemic ca…”

  Formation beats drainage. Raised capillary hydrostatic pressure (left heart failure, the commonest cause) or low plasma oncotic pressure (nephrotic syndrome, hypoalbuminaemia) pushes watery, protein-poor fluid across an intact membrane — a transudate; in cirrhosis a hepatic hydrothorax is mostly ascitic fluid tracking up through small diaphragmatic defects. Inflammation of the membrane from pneumonia, tuberculosis, malignancy or pulmonary infarction makes it leaky to protein and cells, and tumour physically obstructs the lymphatic stomata — an exudate. Either way the fluid pools in the dependent part of the space, compresses the lung and impedes descent of the diaphragm.

  Transudate = a pressure or oncotic problem elsewhere, treat the heart, liver or kidney. Exudate = a pleural problem, find the cause. A parapneumonic effusion that is frankly purulent, culture-positive, or has pleural fluid pH <7.2 (empyema or complicated effusion) needs drainage, not antibiotics alone.

  You would find: Stony dull percussion, absent breath sounds and reduced vocal resonance and tactile fremitus over the fluid, with the trachea and mediastinum pushed away if it is large. An erect chest x-ray blunts the costophrenic angle at roughly 200 mL (a lateral film picks up smaller volumes, of the order of 50 mL); ultrasound detects far less and should guide any tap. Aspirate it and apply the Light criteria — an exudate if any one of pleural:serum protein >0.5, pleural:serum LDH >0.6, or pleural LDH above two-thirds of the upper limit of normal serum LDH. Light's criteria over-call exudate in roughly a quarter of transudates in patients already on diuretics, where a serum-minus-pleural albumin gradient >12 g/L points back to a transudate.

• Pleuritis (pleurisy) and pleuritic chest pain← from “The parietal layer is supplied by ordinary som…”

  Inflammation of the pleural surfaces — pneumonia underneath, lung infarcted against the pleura by a pulmonary embolus, a virus, or an autoimmune disease such as lupus or rheumatoid arthritis — roughens the two layers so they grate instead of gliding. Inflammatory mediators, prostaglandin E₂ prominent among them, sensitise the somatic nerve endings in the parietal layer, so each stretch of the inflamed surface fires them.

  Parietal pleura is somatically innervated, visceral is not — so pleuritic pain means the parietal layer is involved. Sharp, breath-related, point-localised, with a rub. Shoulder tip pain = central diaphragmatic pleura via the phrenic nerve.

  You would find: Sharp pain the patient localises with one finger, worse on deep breath, cough or movement; shallow splinted breathing; a leathery pleural rub on auscultation. Central diaphragmatic pleura refers pain to the shoulder tip through C3–C5, while the peripheral diaphragmatic rim refers to the lower chest and upper abdomen. Pleuritic pain with breathlessness and a clear chest x-ray must trigger formal assessment for pulmonary embolism (validated risk score, then D-dimer or CT pulmonary angiogram) rather than reassurance.

• Malignant pleural mesothelioma← from “Two layers — one stuck to the lung surface (vi…”

  Inhaled asbestos fibres, particularly long thin amphiboles such as crocidolite, are too long and stiff for macrophages to clear. They reach the pleural surface, where decades of frustrated phagocytosis, reactive oxygen species and chronic inflammation drive malignant change in the mesothelial cells lining the space. The tumour spreads as a rind over both layers, encasing the lung, invading the somatically innervated parietal pleura and chest wall, and producing recurrent blood-stained effusion.

  Australia has one of the highest incidences in the world — Wittenoom crocidolite mining, tradespeople, and a later wave among home renovators exposed to asbestos cement. Unexplained exudative effusion plus constant chest wall pain plus an asbestos history: get tissue, and document the occupational exposure history carefully, because statutory compensation depends on it.

  You would find: Persistent dull, constant chest wall pain that is not relieved by draining the fluid, a blood-stained exudative effusion, and nodular or circumferential pleural thickening (especially mediastinal pleural involvement) on contrast CT. Latency from first exposure is long — commonly 30 to 40 years and sometimes longer still — so ask what the patient did for work decades ago. Diagnosis needs tissue, usually image-guided or thoracoscopic biopsy, rather than cytology alone in most cases.

What we give, and how it works

Open a drug to see what it binds, what that does to the cell, and what you then see in the patient.