The superior thoracic aperture ‘(otherwise called thoracic inlet or outlet)’ lies in an oblique transverse plane and connects the thoracic cavity with the root of the neck. Its anteroposterior diameter is 4.5–6 cm and the transverse diameter is 9–11 cm.
Boundaries
Anterior – superior border of manubrium sterni
Posterior – anterior border of the T1 vertebral body
Lateral – medial border of first rib
The superior thoracic aperture lies in an oblique transverse plane (45°) as the first rib slopes downwards and forwards from its posterior end to anterior end. Because of this angle, the apex of the lung and pleura project upward into the neck (Figure 2.1).
Figure 2.1 Thoracic inlet.
What is Sibson’s fascia and what are its functions?
It is a dense fascial sheet otherwise known as the suprapleural membrane, which covers the dome of the pleura. The apex of Sibson’s fascia is connected to the C7 transverse process and its base is connected to the inner border of first rib and its costal cartilage.
Its functions are to
Shield the underlying cervical pleura and the lung apex beneath it
Resist the intrathoracic pressure being transmitted to the neck during respiration
Coming back to the thoracic inlet, name the structures going through it?
Only important structures are listed (Figure 2.2).
Figure 2.2 Thoracic inlet – structures and relations.
Midline and paramedian structures
Sternothyroid muscles
Trachea
Oesophagus
Thoracic duct
Recurrent laryngeal nerve
Lateral structures
Apices of lung and pleurae
Sympathetic trunks
Brachiocephalic/subclavian veins
Vagi and phrenic nerves
Brachiocephalic artery on the right
Common carotid and subclavian arteries on the left
wWhat is its clinical significance?
Thoracic inlet (or outlet) syndrome (TOS) occurs when the above structures get compressed by the scalene muscles, an abnormal rib or by trauma.
Neurogenic TOS – compression of the brachial plexus between the first rib and the scalene muscles. The clinical features include numbness, tingling, wasting and pain along distribution of compressed nerve. The symptoms get worse when the arm is raised overhead.
Venous TOS – compression of the subclavian vein between the clavicle and the first rib causing a thrombus. This is characterised by a sudden swollen and discoloured arm requiring thrombolysis and surgical decompression.
Arterial TOS – compression of the subclavian artery by an anomalous first rib. There could be ischaemic symptoms in the upper limb necessitating urgent surgery.
Inferior thoracic aperture
The inferior thoracic aperture is larger and more oblique than the thoracic inlet and connects the thorax with the abdomen.
Boundaries
Posterior – T12 vertebral body
Posterolateral – 11th and 12th ribs
Anterolateral – costal cartilages of 7th to 10th ribs
Anterior – xiphisternum
Contents
The diaphragm occupies this opening and separates the thoracic and abdominal cavities. So, the structures exiting the inferior outlet are those passing through the diaphragmatic foramina (T8, T10, T12 and other smaller foramina).
The trachea which measures 10–12 cm in length and 2–2.5 cm in width is a semi-cylindrical chondromembranous structure with a flattened posterior aspect. It is comprised of 15–20 cartilages which are incomplete posteriorly, where the oesophagus and trachea share a fibroelastic membrane. It originates at the level of the cricoid cartilage (C6) and terminates by bifurcating into right and left main bronchi at the carina (T4 on expiration and T6 on full inspiration).
Blood supply – inferior thyroid artery and veins
Nerve supply – recurrent laryngeal nerve and sympathetic fibres from middle cervical ganglion
Lymphatic drainage – deep cervical, pretracheal and paratracheal lymph nodes
Relations of the trachea
In the neck – trachea lies in the midline
Anterior: skin, fascia, isthmus of thyroid over 2–4 tracheal rings, sternothyroid and sternohyoid muscles, jugular arch and thyroidea ima artery (if present)
Posterior: oesophagus, recurrent laryngeal nerve in groove between trachea and oesophagus and vertebral bodies
Lateral: thyroid gland, carotid sheath, lung and pleura and great vessels
In the thorax – trachea deviates slightly to the right due to the arch of aorta
Anterior – inferior thyroid veins, the remains of the thymus, brachiocephalic and left common carotid arteries and aortic arch
Posterior – oesophagus and left recurrent laryngeal nerve
Lateral – right: mediastinal pleura, azygous vein and the right vagus nerve
Lateral – left: mediastinal pleura, left common carotid and subclavian arteries, the aortic arch and the left vagus nerve
Discuss how the trachea can be damaged. Describe the mechanisms of injury.
This answer can be broken down in several ways, however the most straightforward option would be to present internal vs external mechanisms of injury.
Internal injury
Inhalation of foreign body
Aspiration of caustic substances including GI contents
Smoke inhalation (burns)
Internal thoracic injury causing rupture/tear
External injury
Trauma (blunt or penetrating)
Compression (strangulation, hanging, haemorrhage in neck compartment)
What is the difference between penetrating and blunt injuries to the trachea?
Penetrating injury – either by sharp instruments or gunshot wound. Usually occur in the cervical region and are associated with involvement of nearby structures such as oesophagus, heart, spinal cord, major vessels and nerves.
Blunt injury – can be due to direct trauma or hyperextension of the neck from motor vehicle accidents. They are associated with extensive injuries to the face, head, chest and abdomen. The mechanism of injury could be due to
Sudden anteroposterior compression leading to disruption of lung at carina
High airway pressure due to compression of chest against a closed glottis causing tracheobronchial rupture
Rapid deceleration injury causing shearing at the fixation sites such as carina and cricoid cartilage
Clothesline injury – compression of trachea between cervical vertebrae (seen in hanging injury)
What are the clinical features of tracheal injury?
The clinical features result from airway injury per se or from associated injuries such as oesophageal injury, haemopneumothorax, major vascular injury, recurrent laryngeal nerve and spinal cord injury.
Signs and symptoms include pain, dyspnoea, drooling, stridor, hissing of air, voice alteration, surgical emphysema (subcutaneous or mediastinal), bleeding, haemoptysis and pneumothorax.
How would you manage tracheal injury? Is it safe to intubate and ventilate?
ABCDE approach – tracheal injury falls under A!
Do NOT forget major haemorrhage control in trauma, i.e. if the carotid artery is bleeding out, compression before intubation is a sensible option.
And always have a plan B!
Airway management is tailored to the type of injury, the nature and extent of airway compromise and haemodynamic and oxygenation status.
Small (<2 cm) mucosal injuries with no associated injuries in patients who are able to breathe spontaneously may be treated conservatively. It is important to identify the point of injury before deciding on airway management. For example, if the injury is proximal to the cricothyroid membrane, a tracheostomy may become plan A. If, however, the injury is distal to the cricothyroid membrane, isolation and one lung ventilation may be necessary.
Blunt tracheal or laryngeal trauma
Clinically blunt injuries are identified by the presence of hoarseness, cough, stridor and associated carotid vascular injury. The presence of subcutaneous emphysema suggests the possibility of airway disruption. Intubation is better performed in the operating theatre with bronchoscopy and cricoid pressure is generally avoided in laryngeal trauma.
Penetrating airway trauma
Direct laryngoscopy with rapid sequence induction or primary surgical airway would be the preferred and successful technique in the management of penetrating neck trauma. Associated great vessel disruption should be recognised/considered and embracing supine or Trendelenburg position can reduce the risk of an air embolism. Again cricoid pressure and positive pressure bag ventilation is avoided until airway is secured. Awake fibreoptic intubation may not be ideal because of the presence of airway oedema, bleeding and secretions or the patient might be obtunded.
You are called to see a 62-year-old male with a history of foreign body inhalation following a dental appointment. He appears comfortable, has mild stridor, normal oxygen saturations and his chest is clear on auscultation. The ENT surgeon is available and would like to perform a rigid bronchoscopy to remove the object.
How would you proceed to anaesthetise this patient?
Foreign body aspiration is a common cause of accidental morbidity and mortality in children under the age of 5 years. In adults, the major causes of foreign body inhalation are altered mental status (sedative use, alcohol, trauma), advanced age (>70 years) and impaired cough reflex (stroke, epilepsy, Parkinson’s disease).
The symptoms depend on size, type and shape of the foreign body, duration and location of airway obstruction and patients could be asymptomatic. In children with cough and stridor with no clear history, alternate diagnosis of croup, acute epiglottitis and acute tracheitis should be excluded.
Signs and symptoms of upper airway obstruction – cough, choking, cyanosis, desaturation, stridor and tachypnoea
Signs and symptoms of lower airway obstruction – respiratory distress, tachypnoea, wheeze and absent breath sounds on the affected side
Organic objects such as peanuts or other food material can elicit an inflammatory process and causes oedema and chemical pneumonitis. Some foreign bodies can get lodged in distal smaller airways and create a ‘ball valve’ effect where in air trapping and distal atelectasis happens.
Complications of airway foreign body
Asphyxia and death
Pneumonia, bronchiectasis and atelectasis
Bronchial stricture and inflammatory polyps
How would you proceed to anaesthetise this patient?
Preassessment and investigations
Rapid yet careful assessment with particular attention to history and airway signs. If the patient is asymptomatic and stable, a chest radiography may be helpful in localising the foreign body although most objects in children are not radio opaque. Chest CT scans can aid further in the diagnosis especially in delayed presentation or patients with chronic respiratory symptoms and reduce the number of unwarranted bronchoscopies.
Premedication and fasting
Anticholinergics are used to decrease airway secretions and reduce vagal tone (bradycardia) during bronchoscopy. Dose in children: atropine 20 mcg/kg or glycopyrrolate 4 mcg/kg.
If the patient is stable with no or minimal distal airway obstruction, optimal fasting times are followed to decrease the risk of aspiration of gastric contents because the airway cannot be fully protected during the procedure.
Choice of anaesthetic induction
Intravenous access and monitoring as per AAGBI guidelines are instituted. It should be borne in mind that EtCO2 monitoring may be inaccurate during the procedure due to leakage of gases around the bronchoscope. Appropriate personnel (senior anaesthetist, skilled anaesthetic assistant and an ENT surgeon) and good communication between all members of staff is vital. Induction of anaesthesia by the inhalation or intravenous route are both described in the literature and depends on personal preference and the experience of the anaesthetist. Whatever the choice of induction may be, spontaneous ventilation must be maintained until it is certain that the patient can still be ventilated post induction. Forced bagging may risk loss of the airway due to fragmentation or dislodgement of the foreign body and may also increase the chance of hyperinflation, pneumothorax and aspiration of gastric contents.
After induction, administration of topical local anaesthetic (1% lignocaine to maximum of 4 mg/kg) to the airway is favourable as it obtunds the airway reflexes and results in a smooth bronchoscopy.
Studies have failed to show the superiority of either mode of ventilation and the outcomes are almost universally good. Breathing circuits can be connected to the sidearm of the rigid bronchoscopes for ventilation.
Jet ventilation is another known method of oxygenation during the procedure and anaesthesia is maintained with intravenous agents.
Procedure
Rigid bronchoscopy is the gold standard, but flexible scopes can be used in children or in diagnostic procedures. Instruments available for foreign body extraction include forceps, snares, baskets, suction catheters, fogarty balloons, magnet catheters and cryotherapy probes.
After the removal of the inhaled foreign body, in the absence of complications, mask ventilation can be applied until adequate spontaneous ventilation is reached.
Postoperative period
Patients are monitored for stridor and airway obstruction due to oedema or procedural complications such as pneumothorax and pneumomediastinum.
If stridor occurs or worsens, nebulised adrenaline 1:1000 and/or intravenous dexamethasone for 24 hours is recommended.
Regular physiotherapy and antibiotics should be prescribed if secondary infection is suspected.
Table 2.1 Comparison of Modes of Ventilation in Patients with Foreign Body Inhalation
Spontaneous ventilation
Mechanical ventilation
Advantages
1.Less risk of dislodgement of foreign body
2.Continuous ventilation throughout procedure
3.Aids in rapid assessment of airway adequacy post retrieval
Advantages
1.Use of muscle relaxant to aid instrumentation
2.Use of balanced anaesthesia with multiple drugs decreases effects on cardiac output
Disadvantages
1.Increased depth of anaesthesia needed for the procedure can cause cardiovascular and respiratory depression.
2.Increased resistance to ventilation during the use of the telescope worsens hypoventilation.
Disadvantages
1.Manual ventilation can dislodge the foreign object more distally requiring difficult retrieval and can convert the proximal partial obstruction to complete obstruction.
2.Increased chance of ball valve effect
If the same patient had presented in extremis with stridor, choking sensation and deteriorating oxygen saturations, how would this change your management?
In witnessed choking, where the patient is conscious, they should be encouraged to cough or external manoeuvres (back blows and chest thrusts in infants and abdominal thrusts in adults and older children) are performed to expel the foreign body.
If the patient is deteriorating, then every attempt should be taken to secure the airway. Immediate endotracheal intubation should be performed, and if the foreign body is seen in the upper airway and can be removed, avoid blind finger sweeps at all times. If intubation fails due to upper airway obstruction from foreign object or airway oedema, difficult airway society (DAS) guidelines should be followed and cricothyroidotomy should be performed.
List the indications for tracheostomy.
Prolonged ventilation/weaning
Failed intubation/extubation
Bronchial toilet/reduce retention of secretions
Airway protection in neurological dysfunction, e.g. bulbar palsy
Domiciliary ventilation in patients with chronic conditions
Reduction of airway complications of long-term intubation
What are the contraindications to bedside tracheostomy?
Absolute – patient refusal, local sepsis, tumour, midline neck swelling or mass
Relative – severe coagulopathy, thrombocytopenia or platelet dysfunction, aberrant vessels in the surgical field, difficult anatomy – short fat or immobile neck or unstable C-spine injury, tracheomalacia
When do you decide about tracheostomy for weaning in ICU?
The timing of tracheostomy in cases of predicted prolonged mechanical ventilation is still controversial. The TracMan (2014) study demonstrated a reduction in days of sedation but this was not translated into a reduction in mortality, hospital stay or ICU stay. In summary, there is no demonstrated advantage to early tracheostomy in those patients that will predictably need prolonged ventilation, therefore each case is dealt with individually.
How will you perform a percutaneous tracheostomy?
Consent
Assessment of neck (ultrasound may be useful)
Monitoring including capnography; trained assistant; equipment
Bronchoscopy to visualise larynx above level of carina
Palpation and local anaesthetic infiltration below second or third tracheal rings
Seldinger technique to insert percutaneous tracheostomy (Note: there are multiple techniques, see below. Choose one that you are familiar with.)
Secure airway device
X-ray to rule out complications and confirm positioning
What are the potential complications of tracheostomy?
Immediate – cuff herniation, vascular damage resulting in bleeding, tracheal trauma, loss of airway, other neck trauma (thyroid), surgical emphysema and pneumomediastinum
Early – haematoma formation, pneumothorax, haemothorax, infection, false passage formation, tracheostomy displacement, blockage and tracheo-oesophageal fistula
Late – recurrent laryngeal nerve damage, tracheal stenosis, tracheal granulomata, swallowing difficulties and tracheomalacia
What techniques are available for insertion of a percutaneous tracheostomy?
Percutaneous dilatational method with multiple dilators for graduated dilatation (Ciaglia)
Percutaneous dilatational technique with single dilator (Rhino)
Guidewire and dilating forceps (Grigg’s forceps)
Other (Portex ULTRAperc, etc.)
What are the anaesthetic considerations for a patient with long-term tracheostomy?
This can be discussed under the following headings.
Reason for tracheostomy – difficult airway, pulmonary toilet, prolonged ICU stay and neurological dysfunction
Presence of co-morbid diseases – ICU patient with multi-organ failure, sepsis, lung injury, neuromuscular disorders and chronic high spinal cord injury
Dealing with the potential complications of long-term tracheostomy (as discussed earlier)
Risk of loss of airway – various sizes of cuffed/uncuffed tracheostomy tubes, suction catheters, graspers, ambu bag and ties should be available in case of loss of airway. Additionally, a difficult airway trolley should be available for rescue.
Practical tracheostomy management – suction prior to induction, removal of inner tube, connection to breathing circuit for preoxygenation +/– gas induction, inspection of EtCO2 and spirometry loops
Bronchial Tree
The right and left main bronchi originate at the carina. The right main bronchus is shorter (2.5 cm vs 5 cm), wider and more vertical to the midline (25° vs 45°). This structure has a couple of clinical implications in anaesthesia (Figure 2.4).
Endobronchial intubations are, more often than not, on the right side.
Foreign bodies traversing the trachea are more likely to enter the right side.
During use of a right-sided double lumen tube, careful positioning and confirmation with a fibreoptic scope is necessary to prevent occlusion of the right upper lobe bronchus arising at 2.5 cm.
The bronchi undergo 23 divisions (16 – conducting zone or a conduit where there is no gas exchange; 7 – respiratory zone) and it is listed in Table 2.2.
Figure 2.4 Tracheobronchial tree.
Table 2.2 Generations of the Tracheobronchial Tree
Lungs are conical structures, where the right is heavier and larger but shorter than the left. The apex of the lung lies at the root of neck with the tip extending 4 cm above the medial one third of the clavicle making it prone to iatrogenic damage whilst performing supraclavicular brachial plexus blocks or subclavian venous cannulation. The base of the lung rests on the diaphragm and the right base is placed higher than the left by the presence of the liver.
Fissures
The right lung is divided into three lobes by the oblique and horizontal fissures whilst the left has two lobes formed by the oblique fissure.
Oblique fissure – divides the lower lobe from the upper and middle lobes
Posteriorly – starts at T5 vertebral body, then follows the direction of the fifth rib
Anteriorly – ends at sixth costochondral junction (T5 → 5th rib → 6th CC junction)
Horizontal fissure – delineates the upper and middle lobe
Anteriorly – starts at right fourth costochondral junction and runs transversely backwards and meets the oblique fissure in the midaxillary line at the level of the fifth rib (4th CC junction → 5th rib)
Broncho pulmonary segments
The bronchopulmonary segments (ten segments on each side) are well defined functional areas of lung supplied by a segmental or tertiary bronchus. Each segment is pyramidal in shape serving as an individual respiratory unit with its own pulmonary arterial supply; the pulmonary venous circulation running in the intersegmental plane (Figure 2.5).
Figure 2.5 Bronchopulmonary segment.
The clinical importance of these segments are listed below.
Segmental resection can be carried out with minimal disruption to the surrounding lung tissue.
Visualisation with bronchoscopes can delineate the affected lung when the disease process is limited to particular segments.
Root of lung
The root or stalk connects the lung to the heart and trachea and hilum is the opening in the pleural sheath that transmits the structures constituting the root (pulmonary artery, pulmonary veins, the bronchi, bronchial vessels, lymph nodes and autonomic nerves).
Relations at the lung hilum
Anterior – phrenic nerve, superior vena cava, anterior pulmonary plexus and part of right atrium (right lung)
Posterior – vagus nerve and posterior pulmonary plexus
Superior – aortic arch and azygos vein
Inferior – pulmonary ligament
How is the right hilum different from the left?
The relationships of the roots of the right and left lung are different because of the structures that make them and their position at the hila (Figures 2.6, 2.7 and Table 2.3).
Figure 2.6 Right hilum.Figure 2.7 Left hilum.
Table 2.3 Comparison of the Right and Left Lung Hilum
Right hilum
Left hilum
One pulmonary artery (anterior and above)
One pulmonary artery (anterior and above)
Two pulmonary veins (below the artery)
Two pulmonary veins (below the artery)
One upper lobar bronchus (ep-arterial or above pulmonary artery)
One bronchus intermedius (hyp-arterial or below pulmonary artery)
One main bronchus (hyp-arterial or below pulmonary artery)
One bronchial artery (posterior to bronchi)
Two bronchial arteries (posterior to bronchus)
Other structures
Bronchial veins, anterior and posterior pulmonary nerve plexus, areolar tissue and bronchopulmonary lymph nodes
Other structures
Bronchial veins, anterior and posterior pulmonary nerve plexus, areolar tissue and bronchopulmonary lymph nodes
What type of nerves supply the lung tissue?
Sensory
Fibres sensitive to stretch of lung (vagus nerve)
Pain fibres from parietal pleura (phrenic and intercostal nerves)
Sympathetic
Bronchodilatory fibres (T2–T4)
Parasympathetic
Bronchoconstrictor fibres (Vagus)
Secretomotor fibres to the mucous glands
Discuss the blood supply to the lung and adjoining connective tissue.
The blood supply to the lung is via the bronchial circulation which, as previously discussed, forms part of the systemic circulation. It comprises 1–2% of the total cardiac output.
Bronchial arteries
Left bronchial arteries – there are two left-sided bronchial arteries (superior and inferior) which arise from the thoracic aorta at the level of the T5 and T6 vertebrae.
Right bronchial artery – the origin of the single right bronchial artery may vary. It may arise directly from the thoracic aorta, from a common trunk shared with the left bronchial artery, or from a right-sided posterior intercostal artery.
The bronchial arteries supply blood to the bronchi and connective tissue of the lungs. They terminate at the level of the respiratory bronchioles by way of an anastomosis with the pulmonary arteries and together, they supply the visceral pleura.
Bronchial veins
The bronchial veins run alongside the bronchial arteries, but they only carry ~13% of the bronchial venous blood to the systemic venous circuit.
Two types of bronchial veins that exist are the deep and the superficial veins and both communicate freely with the pulmonary veins. The superficial bronchial veins from the larger airways and hilum drain into the systemic veins (azygos vein, left superior intercostal vein and the accessory hemiazygos vein) and then into the right atrium. The deep veins originate from the terminal bronchioles and drain into the left atrium directly or via the pulmonary veins constituting the ‘anatomical shunt’ (1–2% of cardiac output) desaturating the left atrial blood to 99%.
Pulmonary circulation
There are two pulmonary arteries (left and right) that carry deoxygenated blood from the right ventricle to the lung and four pulmonary veins that carry oxygenated blood to the left atrium.
Two main pulmonary veins emerge from each lung hilum, receiving blood from bronchial veins and draining into the left atrium. An inferior and superior pulmonary vein drains each lung, giving four main pulmonary veins in total.
At the root of the lung, the right superior pulmonary vein lies anterior to the pulmonary artery; the inferior is situated at the lower most part of the lung hilum. The right main pulmonary veins pass posterior to the right atrium and superior vena cava; the left anterior to the descending thoracic aorta.
Please see the section on Pulmonary Circulation for further reading.
What is suprapleural membrane (Sibson’s fascia) and what is its importance?
The suprapleural membrane is the dense fascial structure that is said to be flattened tendon of the scalenus minimus muscle. Its function is to provide rigidity to the thoracic inlet and prevent the changes in intrathoracic pressure during respiration causing distortion of neck structures. Also, it protects the underlying cervical pleura, and the apex of the lung beneath it. The subclavian vessels lie above the fascia.
Attachments
Anterior – inner border of the first rib and costal cartilage
Posterior – C7 transverse process
Medial – mediastinal pleura
Lateral – medial margin of the first rib
Inferior – blends with the dome of cervical 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?
Pleural fluid is a clear ultrafiltrate of plasma.
Quantity: 0.2 ml/kg (8.4 +/– 4.3 ml)
Cellular contents: 75% macrophages and 25% lymphocytes
Biochemistry: compared to plasma, the pleural fluid is alkaline (pH @ 7.6) with higher albumin content but lower sodium, chloride and LDH.
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 and internal mammary vessels. Venous drainage is via the intercostal veins and azygos veins, finally draining into the SVC and IVC.
How is pleura innervated?
The visceral pleura does not have pain fibres but responds to stretch and is supplied by the pulmonary branch of vagus nerve and the sympathetic trunk.
The parietal pleura receives an extensive innervation from the somatic intercostal and phrenic nerves.
Explain 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.
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