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Respiratory Failure
Respiratory failure occurs when the respiratory system fails in oxygenation and/or carbon
dioxide (CO2) elimination. Respiratory failure may be:

Hypoxaemic respiratory failure (type I respiratory failure): PaO2 is less than 60 mm

Hg (8 kPa) with a normal or low PaCO2. This is caused by ventilation-perfusion
mismatch with either/both:
o Under-ventilated alveoli (eg pulmonary oedema, pneumonia or acute asthma).
o Venous blood bypasses ventilated alveoli (eg right to left cardiac shunts).

Hyperventilation increases CO2 removal but does not increase oxygenation, as blood
leaving unaffected alveoli is almost fully saturated.

Hypercapnic respiratory failure (type II respiratory failure): PaCO2 is more than 50

mm Hg (6.5 kPa) and indicates inadequate alveolar ventilation. Any ventilation-perfusion
mismatch will affect PaO2 and therefore hypoxaemia is also common.

Respiratory failure may be acute or chronic:

Acute hypercapnic respiratory failure develops over minutes to hours. The pH is usually
therefore less than 7.3.
Chronic respiratory failure develops over several days or longer. There is sufficient time
for renal compensation and an increase in bicarbonate so the pH is usually only slightly
decreased. Clinical markers of long-standing hypoxaemia include polycythaemia and cor

Common causes of type I respiratory failure
Chronic obstructive pulmonary disease (COPD).
Pulmonary oedema.
Pulmonary fibrosis.
Pulmonary embolism.
Pulmonary hypertension.
Cyanotic congenital heart disease.
Acute respiratory distress syndrome.

Common causes of type II respiratory failure

Severe asthma.
Drug overdose.
Myasthenia gravis.
Muscle disorders.
Head injuries and neck injuries.
Pulmonary oedema.
Adult respiratory distress syndrome.

The history may indicate the underlying cause, eg paroxysmal nocturnal dyspnoe, and
orthopnoe in pulmonary oedema.
Both confusion and reduced consciousness may occur.

Localised pulmonary findings are determined by the underlying cause.
Neurological features may include restlessness, anxiety, confusion, seizures, or coma.
Tachycardia and cardiac arrhythmias may result from hypoxaemia and acidosis.
Polycythaemia is a complication of long-standing hypoxaemia.
Cor pulmonale: pulmonary hypertension is frequently present and may induce right
ventricular failure, leading to hepatomegaly and peripheral oedema.


A patient with acute respiratory failure generally needs prompt hospital admission in an intensive
care unit. Many patients with chronic respiratory failure can be treated at home, depending on
the severity of respiratory failure, underlying cause, comorbidities and social circumstances.

Immediate resuscitation may be required.

Appropriate management of the underlying cause.

Ensure adequate oxygen delivery to tissues, generally achieved with a PaO2 of 60 mm Hg
or an arterial oxygen saturation (SaO2) of greater than 90%.
Beware the prolonged use of high-concentration oxygen in chronic sufferers who have
become reliant on their hypoxic drive to maintain an adequate ventilation rate. Elevating
the PaO2 too much may reduce the respiratory rate so that the PaCO2 may rise to
dangerously high levels.
Assisted ventilation:
o Mechanical ventilation is used to increase PaO2 and to lower PaCO2. Mechanical
ventilation also rests the respiratory muscles and is an appropriate therapy for
respiratory muscle fatigue. Weaning patients with chronic respiratory failure off
of mechanical ventilation may be very difficult.
o Non-invasive ventilation (NIV) has been increasingly used as an alternative to
intubation. NIV improves survival and reduces complications for selected patients
with acute respiratory failure. The main indications are exacerbation of COPD,
cardiogenic pulmonary oedema, pulmonary infiltrates in immunocompromised
patients, and weaning of previously intubated stable patients with COPD.
Hypercapnia and respiratory acidosis

Correct the underlying cause and/or provide assisted ventilation.

Pulmonary: for example, pulmonary embolism, pulmonary fibrosis, and complications
secondary to the use of mechanical ventilation.
Cardiovascular: for example, cor pulmonale, hypotension, reduced cardiac output,
arrhythmias, Gastrointestinal: for example, haemorrhage, gastric distention, ileus,
diarrhoea, and pneumoperitoneum. Polycythaemia.
Hospital-acquired infection: for example, pneumonia, urinary tract infections, and
catheter-related sepsis, are frequent complications of acute respiratory failure.
Renal: acute kidney injury (acute renal failure) and abnormalities of electrolytes and
acid-base balance are common in critically ill patients with respiratory failure.
Nutritional: including malnutrition and complications related to administration of enteral
or parenteral nutrition. Complications associated with nasogastric tubes, eg abdominal
distention and diarrhoea.

Acute Severe Asthma and Status Asthmaticus

When the diagnosis of asthma is confirmed and comorbidities addressed, severe asthma is
defined as asthma that requires treatment with high-dose inhaled corticosteroids plus a second
controller and/or systemic corticosteroids to prevent it from becoming 'uncontrolled' or that
remains 'uncontrolled' despite this therapy.

Asthma is a common disease and its frequency sometimes detracts from its potential seriousness.
In adults with asthma, only 5-10% have severe disease but these individuals carry a substantial
proportion of the cost (both in terms of morbidity and economic consideration) and run the
highest risk of acute severe exacerbations and death.

Status asthmaticus is severe asthma that does not respond well to immediate care and is a life-
threatening medical emergency. Ensuing respiratory failure results in hypoxia, carbon dioxide
retention and acidosis. The exact mechanism underlying the development of an acute severe
asthma attack remains elusive but there appear to be two phenotypes:

Gradual-onset - in about 80%, severe attacks develop over more than 48 hours. These are
associated with eosinophilic infiltration and slow response to therapy.
Sudden-onset - often in association with significant allergen exposure. Patients tend to be
older and to present between midnight and 8 am. This type of attack is associated with
neutrophilic inflammation and a swifter response to therapy.

In deaths from asthma there is often a failure to recognise the full severity of the situation. This
can be down to the patient, their family/carers or the healthcare team but often a multitude of
factors is involved. Patients frequently have adverse psychosocial factors that interact with the
ability to judge or manage their disease or have a diminished perception of their dyspnoea that
leads to late presentation. Medical care continues to fail sometimes to treat acute severe asthma
aggressively enough or to comply with national guidelines.

Every emergency consultation for asthma should be regarded as for acute severe asthma*
until proven otherwise.
All patients with acute severe asthma* that has not responded to immediate treatment or
life-threatening asthma* must be referred to hospital.

There were 1,167 deaths from asthma in the UK in 2011.
An estimated 75% of admissions for asthma are avoidable and as many as 90% of the
deaths from asthma are thought to be preventable.

Shortness of breath may develop over hours or days but is usually progressive rather than
A history of poor control is common.
Often there has been a recent increase in use of reliever inhalers, with decreasing
Possible respiratory tract infection or exposure to an allergen or trigger.

The patient will usually appear pink. Cyanosis is a serious sign.
Their respiratory rate is raised.
Tachycardia is usual and may be increased by use of beta2 agonists.
Accessory muscles of respiration are employed (best assessed by palpation of the neck
muscles) and the chest appears hyper-inflated.
In normal breathing, the ratio of the duration of inspiration to expiration is about 1:2 but,
as asthma becomes more severe, the expiratory phase becomes relatively more
Wheeze is usually expiratory, but may also be inspiratory in more severe asthma.

Differential diagnosis

Status asthmaticus must be distinguished from other causes of acute breathlessness, including:

Wheezing in children, which can be caused by a variety of infective conditions - eg,

respiratory syncytial virus - causing bronchiolitis.
Foreign body inhalation and other causes of stridor (eg, epiglottitis, croup, tracheitis,
vascular ring, tracheomalacia, etc).
Allergic reaction, anaphylaxis.
Primary pulmonary hypertension.
Pneumothorax with or without asthma.
Inhalation injury.
Acute exacerbations of Chronic obstructive pulmonary disease.
Lung cancer.
Cardiac failure ('cardiac asthma').

Initial treatment
Consider the need for immediate transfer to hospital.
Give supplementary oxygen to all hypoxaemic patients with acute severe asthma to
maintain an SpO2 level of 94-98%. Lack of pulse oximetry should not prevent the use of
Beta2 agonist bronchodilators:
o Outside hospital, high-dose beta2 agonists may be given via large spacer devices
(4-10 puffs inhaled individually) or nebulisers once available (this should be
oxygen-driven where available). Repeat doses of beta2 agonists at 15- to 30-
minute intervals. There is no evidence for any difference in efficacy between
salbutamol and terbutaline.
o Higher bolus doses (eg, 10 mg of salbutamol) are unlikely to be more effective.
o Reserve intravenous beta2 agonists for those patients in whom inhaled therapy
cannot be used reliably.
o For adults with severe asthma that is poorly responsive to an initial bolus dose of
beta2 agonist, consider continuous nebulisation of salbutamol at 5-10 mg/hour
with an appropriate nebuliser. Continuous nebulised beta2 agonists are of no
greater benefit than the use of frequent intermittent doses in the treatment of
children with acute asthma.
Ipratropium bromide:
o Add nebulised ipratropium bromide (0.5 mg 4- to 6-hourly) to beta2 agonist
treatment for adults with acute severe or life-threatening asthma, or those with a
poor initial response to beta2 agonist therapy.
o Corticosteroids reduce mortality and should be given as early in the acute attack
as possible. Give steroids in adequate doses in all cases of acute asthma. Steroid
tablets are as effective as injected steroids, provided they can be swallowed and
o Give oral prednisolone in all cases of acute asthma attack in adults. Higher doses
of steroids don't appear to have any advantage.
o Continue prednisolone 40-50 mg daily for at least five days or until recovery.
Consider giving an infusion of IV magnesium sulfate (only after consultation with senior
medical staff) for patients with life-threatening or near-fatal asthma, or with acute severe
asthma who have not had a good initial response to inhaled bronchodilator therapy.
Antibiotics are not routinely indicated.


Complications of status asthmaticus include:

Aspiration pneumonia.
Respiratory failure and arrest.
Cardiac arrest.
Hypoxic-ischaemic brain injury.

The risk of death is increased where there is delay in getting treatment, particularly time to
starting steroids, comorbidities such as congestive heart failure or COPD and in smokers.
Mortality is highest in the very young and the very old.

Choking and Foreign Body Airway

Obstruction (FBAO)
Choking is the physiological response to sudden airways obstruction. Foreign body airway
obstruction (FBAO) causes asphyxia and is a terrifying condition, occurring very acutely, with
the patient often unable to explain what is happening to them. If severe, it can result in rapid loss
of consciousness and death if first aid is not undertaken quickly and successfully. Immediate
recognition and response are of the utmost importance.

Choking due to inhalation of a foreign body usually occurs whilst eating; it need not have been a
formal 'sit-down' meal - a snack eaten 'on-the-go' or chewing gum can also be inhaled.


Because recognition is the key to successful outcome, it is important to ask the conscious victim
"Are you choking?". This at least gives the victim who is unable to speak the opportunity to
respond by nodding!

Consider the diagnosis of choking particularly if:

Episode occurs whilst eating, and onset was very sudden.

Adult victim - may clutch his or her neck, or points to throat.
Child victim - there may be clues, eg seen eating or playing with small items just before
onset of symptoms.

Assess severity
Mild obstruction:
o The patient is able to breathe, cough effectively and speak.
o Children are fully responsive, crying or verbally respond to questions, may have
loud cough (and able to take a breath before coughing).

Severe obstruction is indicated by:

o Victim unable to breathe or speak/vocalise.
o Wheezy breath sounds.
o Attempts at coughing are quiet or silent.
o Cyanosis and diminishing conscious level (particularly in children).
o Victim unconscious.


In mild obstruction, encourage the patient to continue coughing, but do nothing else
except monitor for deterioration.
In severe obstruction in a conscious patient:
o Stand to the side and slightly behind the victim, support the chest with one hand
and lean the victim well forwards (so that the obstructing object comes out of the
mouth rather than going further down the airway).
o Give up to five sharp back blows between the shoulder blades with the heel of
your other hand (checking after each if the obstruction has been relieved).
o If unsuccessful, give up to five abdominal thrusts. Stand behind the victim (who is
leaning forward) put both arms around the upper abdomen and clench one fist,
grasp it with the other hand and pull sharply inwards and upwards.
o Continue alternating five back blows and five abdominal thrusts until successful
or the patient becomes unconscious.

In an unconscious patient:

o Lower the patient to the floor.

o Call an ambulance immediately.
o Begin CPR (even if a pulse is present in the unconscious choking victim).

If coughing effectively, just encourage the child to cough, and monitor continuously.
If coughing is, or is becoming, ineffective, shout for help and assess the child's conscious
If the child is conscious, give up to five back blows, followed by five chest thrusts to
infants or five abdominal thrusts to children (repeat the sequence until the obstruction is
relieved or the patient becomes unconscious).
o For infants (<1 year old): back blows and chest thrusts:
In a seated position, support the infant in a head-downwards, prone
position to let gravity aid removal of the foreign body.
Support the head by placing the thumb of one hand at the angle of the
lower jaw, and one or two fingers from the same hand at the same point on
the other side of the jaw. Do not compress the soft tissues under the jaw, as
this will aggravate the airway obstruction.
Deliver up to five sharp blows with the heel of your hand to the middle of
the back (between the shoulder blades).
After each blow, assess to see if the foreign body has been dislodged and,
if not, repeat the manoeuvre up to five times.
After five unsuccessful back blows, use chest thrusts: turn the infant into a
head-downwards supine position by placing your free arm along the
infant's back and encircling the occiput with your hand. Support the infant
down your arm, which is placed down (or across) your thigh. Identify the
landmark for chest compression. This is the lower sternum, about a
finger's breadth above the xiphisternum. Deliver five chest thrusts. These
are similar to chest compressions for CPR, but sharper in nature and
delivered at a slower rate.
o For children (1 year old to puberty): back blows and abdominal thrusts:
Blows to the back are more effective if the child is positioned head down.
A small child can be placed across the lap as with an infant. If this is not
possible, support the child in a forward-leaning position.
Deliver up to five sharp back blows with the heel of one hand in the
middle of the back between the shoulder blades.
After five unsuccessful back blows, abdominal thrusts may be used in
children over 1 year old:
Stand or kneel behind the child, placing arms around torso. Placed
clenched fist between the umbilicus and xiphisternum (ensuring no
pressure is applied to either landmark).
Grasp this hand with your other hand and pull sharply inwards and
upwards, repeating up to 5 times.
If the child becomes unconscious, place him or her on a flat, firm surface, shouting for
help if none has arrived. Open the mouth and look for any obvious object. If one is seen,
make an attempt to remove it with a single finger sweep (don't do blind finger sweeps).
If unsuccessful, begin CPR.

Differential diagnosis

Rapid evaluation is key: swiftly consider other conditions that may cause sudden respiratory
distress, cyanosis or loss of consciousness, such as:

Myocardial infarction

Inhaled foreign body: after successful treatment for choking, foreign material may still
be present in the upper or lower airways and cause complications such as bronchiectasis
or lung abscess later. Anyone with a persistent cough, difficulty swallowing, or with the
sensation of an object being still stuck in the throat should therefore be referred to A&E.
CXR may show an opacity that requires removal at bronchoscopy or atelectasis. In
children, clinical features and radiological findings may have a poor correlation with
findings at bronchoscopy. If a foreign body is suspected, bronchoscopy should be
performed at an early stage for best results.
Iatrogenic: abdominal thrusts can cause serious injuries (eg gastric and splenic rupture)
and all victims receiving abdominal thrusts require examination of the abdomen with a
particular view to visceral injuries.
Hypoxic brain injury and death.

A pneumothorax refers to a collection of air in the pleural cavity (between the lung and the chest
wall) resulting in collapse of the lung on the affected side. The extent of the collapse of the lung
is dependent upon the amount of air that is present. Pneumothoraces can be classified into:

Primary spontaneous pneumothorax: pneumothorax occurring in healthy people.

Secondary pneumothorax:
o Associated with underlying lung disease - eg, rupture of a congenital bulla or a
cyst in chronic obstructive pulmonary disease (COPD).
o The consequences of a pneumothorax in patients with pre-existing lung disease
are significantly greater and the management is potentially more difficult.

Other causes of a pneumothorax may include:

Traumatic pneumothorax follows a penetrating chest trauma such as a stab wound,

gunshot injury or a fractured rib.
Iatrogenic pneumothorax may follow a number of procedures such as mechanical
ventilation and interventional procedures such as central line placement, lung biopsy and
percutaneous liver biopsy.
Catamenial pneumothorax refers to pneumothorax at the time of menstruation The
aetiology is endometriosis. It represents 3-6% of spontaneous pneumothorax in women.
Patients are typically aged 30-40 years with a history of pelvic endometriosis in 20-40%.
Over 90% occur in the right lung and it occurs within 72 hours from the onset of
menstruation. In women receiving hormonal treatment, 50% will have a recurrence
within a year.

Tension pneumothorax

Tension pneumothorax is a life-threatening emergency that requires instant action. Severe

symptoms and signs of respiratory distress suggest the presence of tension pneumothorax.

Treatment is with oxygen and emergency needle decompression.

Insert a large-bore needle into the pleural space through the second or third anterior
intercostal space. A gush of air confirms the diagnosis. A standard cannula may be
insufficiently long if used in the second intercostal space.
Typical clinical situations where tension pneumothorax arises include:
o Ventilated patients
o Trauma patients
o Resuscitation patients (CPR)
o Lung disease, especially acute presentations of asthma and COPD
o Blocked, clamped or displaced chest drains
o Patients receiving non-invasive ventilation
o Patients undergoing hyperbaric oxygen treatment


Symptoms in PSP may be minimal or absent. In contrast, symptoms are greater in SSP, even if
the pneumothorax is relatively small in size.

Sudden onset of pain is typical.

There may well be some shortness of breath, depending upon the size of the lesion. It
tends to be more severe in secondary pneumothorax as there is less reserve.
Around two thirds of patients will have both pain and dyspnoea. However, a significant
number may have no symptoms and thus a high index of suspicion is needed.

The patient often looks distressed and is sweating. Dyspnoea may be apparent and even
cyanosis, depending upon the degree of respiratory inadequacy.
Pulse examination:
o Tachycardia is common but a pulse rate above 135 beats per minute suggests
tension pneumothorax.
o Pulsus paradoxicus suggests a severe pneumothorax. Pulsus paradoxicus occurs
when the pulse slows on inspiration. This is the opposite to sinus arrhythmia
where there is a slight acceleration of the pulse with inspiration.
Hypotension may occur and jugular venous pressure (JVP) may be raised, especially in
tension pneumothorax.
Examination of the chest:
o May show that the affected side moves less than the normal side. The best way to
elicit this is to place your hands on each side of the patient's chest and to feel the
movement when you ask him or her to take a deep inspiration.
o The trachea is deviated away from the side of collapse especially in tension
o Percussion reveals hyper-resonance over the collapse.
o Breath sounds are reduced or absent over the affected area.
o Bilateral pneumothorax is unusual but the lack of asymmetry of the chest will
make clinical diagnosis more difficult.
There are specific problems for those who are being ventilated. High peak airway
pressure suggests an impending pneumothorax. There will be difficulty ventilating the
patient during resuscitation. A tension pneumothorax causes progressive difficulty with
ventilation, as the normal lung is compressed.

o Standard erect CXRs in inspiration are recommended for the initial diagnosis of
o Lateral X-rays may provide additional information when a suspected
pneumothorax is not confirmed by a PA chest film. However, they are no longer
used routinely.
o Expiratory films are not thought to confer any additional benefit in the routine
assessment of pneumothorax.
o Specific features on ultrasound scanning are diagnostic of pneumothorax but the
main value of ultrasound has been in the management of supine trauma patients.
o However, ultrasound has been shown in one study to be more accurate than CXR
for detection of pneumothorax.
CT scanning is recommended for uncertain or complex cases.
Arterial blood gases will show hypoxia, the degree being dependent upon the severity of
the condition. It tends to be more disturbed in SSP, as there is less reserve in the presence
of pre-existing lung disease. They probably only need to be done if oxygen saturations
are <92%.

The size of the pneumothorax determines the rate of resolution and is a relative indication for
active intervention. To calculate the size of a pneumothorax: There are various methods that one
can use, but the technique recommended by the British Thoracic Society is to measure the
distance between the pleural surface and the lung edge (at the level of the hilum). If this is 2 cm
or more, it represents a pneumothorax of at least 50% of the hemithorax and is an indication for
drainage. However, in order to determine a management strategy the clinical situation also needs
to be taken into account.

Differential diagnosis
Pleural effusion tends to be slower in onset and there is dullness on percussion.
Chest pain: a pleuritic pain may give a sensation of breathlessness.
Pulmonary embolism may produce haemoptysis and a few rales over the affected area. It
more commonly affects the lower rather than the upper lungs.


Tension pneumothorax requires immediate attention.

Simple observation, needle aspiration and chest drain are all possibilities and the choice will
depend upon the severity of the condition. There is much national and international controversy
surrounding the most appropriate initial treatment of pneumothoraces, especially those <50%.

Generally, the more symptomatic the patient, the more active intervention should be utilised.
Large pneumothoraces should usually be drained, even if there are minimal or no symptoms, as
this speeds the resolution. However, expanding the lung has adverse effects on stopping the air
leak, and so observation without rapidly expanding the lung may be the best management. It has
been reported that conservative management of even large pneumothoraces is possible if there is
no underlying lung disease.

For those patients admitted to hospital, referral to a respiratory physician should be made within
24 hours of admission.


Patients with a small PSP without breathlessness should be considered for discharge with early
outpatient review. These patients should also receive clear written advice to return in the event of
worsening breathlessness.

A small pneumothorax of 15% or less can be managed by observation, using both clinical
assessment and CXR to ascertain that it is not enlarging.
Iatrogenic pneumothorax does not normally require a chest drain.
There is currently insufficient evidence to determine whether any particular intervention
is more effective than no intervention for spontaneous pneumothorax.
Breathlessness indicates the need for active intervention as well as supportive treatment
(including oxygen).

Simple aspiration

Indications for simple aspiration, also called thoracentesis, include PSP (any size) and small SSP
in patients aged under 50 years.

Needle (14-16 G) aspiration is as effective as large-bore (>20 F) chest drains and may be
associated with reduced hospitalisation and length of stay.

The puncture site is commonly in the second or third intercostal space in the
midclavicular line or in the fourth or fifth intercostal space over the superior rib margin in
the anterior axillary line.
Entry should be just above a rib rather than just below it so as to reduce the risk of hitting
the neurovascular bundle.
Aspiration can even be used without admitting the patient to hospital but all patients who
have had a pneumothorax should receive written instructions that if they develop sudden
shortness of breath they must return immediately.
Needle aspiration should not be repeated unless there were technical difficulties.
Following failed needle aspiration, a small-bore (<14 F) chest drain insertion is

There is no significant difference between simple aspiration and intercostal tube drainage with
regard to the immediate success rate, early failure rate, duration of hospitalisation, one-year
success rate and the number of patients requiring pleurodesis at one year. Simple aspiration is
associated with a reduction in the proportion of patients hospitalised when compared with
intercostal tube drainage.

Intercostal tube drainage

A chest drain tube is usually required for SSP and for all large lesions. Chest drains are usually
required for patients with tension or bilateral pneumothorax who should be admitted to hospital.

Indications for a chest drain for pneumothorax include:

In any ventilated patient.

Tension pneumothorax after initial needle relief.
Persistent or recurrent pneumothorax after simple aspiration.
Large SSP in patients aged over 50 years.

Pain, intrapleural infection, wound infection, drain dislodgement and drain blockage are the most
frequent complications of chest drain insertion. Visceral injury is the most serious complication.

Antibiotic prophylaxis is not recommended for non-trauma patients requiring a chest drain.
Antibiotic prophylaxis should be considered for trauma patients requiring chest drains, especially
after penetrating trauma.

There are concerns regarding the development of re-expansion pulmonary oedema. It is therefore
recommended that suction should not be used routinely. Caution is required because of the risk
of re-expansion pulmonary oedema. High-volume low-pressure suction systems are

If there has been recurrence or the risk is considered high then prevention of further
pneumothorax by pleurodesis should be considered.
Medical pleurodesis may be appropriate for inoperable patients. Chemical pleurodesis
can control difficult or recurrent pneumothoraces but, since surgical options are more
effective, it should only be used if a patient is either unwilling or unable to undergo
Complications include failure to prevent recurrence, acute respiratory distress, infection
of the pleural space, persistent air leak and re-expansion pulmonary oedema.
Simple aspiration and drainage followed by minocycline pleurodesis has been shown to
be safe and possibly more effective treatment for PSP than simple aspiration and drainage
Pleural abrasion with minocycline pleurodesis has also been shown to be as effective as
apical pleurectomy and it is therefore recommended that either technique is appropriate
for treating PSP patients with high recurrence risk.
One review found that, although the relative risk of recurrence was higher with pleural
abrasion compared to pleurectomy, it was not statistically significant.

For more difficult cases referral to thoracic surgeons may be considered.
An early (3-5 days) thoracic surgical opinion should be sought in cases of persistent air
leak or failure of the lung to re-expand.
Open thoracotomy and pleurectomy remains the procedure with the lowest recurrence
rate (approximately 1%) for difficult or recurrent pneumothoraces.
Video-assisted thoracoscopic surgery (VATS) with pleurectomy and pleural abrasion is
better tolerated but has a higher recurrence rate of approximately 5%.
Surgical chemical pleurodesis is best achieved by using sterile graded talc, which only
rarely causes acute respiratory distress syndrome and empyema.

Haemoptysis is the coughing of blood originating from the respiratory tract below the level of
the larynx. Haemoptysis should be differentiated from:

Haematemesis - vomiting of blood from the gastrointestinal (GI) tract.

Pseudohaemoptysis - where a cough reflex is stimulated by blood not derived from the
lungs or bronchial tubes. This may be from the oral cavity or nasopharynx (eg, following
an epistaxis) or following aspiration of haematemesis into the lungs.

Classifications of severity vary. Although volumes of 100 to 1000 mL of blood have been
described as indicative of massive haemoptysis, no specific volume has been universally
accepted. However, a large volume of expectorated blood alone should not define massive
haemoptysis, but rather an amount of blood sufficient to cause a condition that threatens the
patient's life is usually a more correct and functional definition of severe haemoptysis. [1]

According to source of bleeding:

Trachea or bronchus
o Bronchogenic carcinoma.
o Endobronchial metastatic tumour.
o Kaposis sarcoma.
o Carcinoid tumour.
Airway trauma.
Foreign body.

Lung parenchyma
Lung abscess.
Pneumonia - bacterial (eg, Staphylococcus aureus, Pseudomonas aeruginosa) or viral
(eg, influenza).
Fungal infection and mycetoma.
Hydatid cysts.
Goodpasture syndrome.
Pulmonary haemosiderosis.
Wegener granulomatosis.
Bechet disease.
Lupus pneumonitis.
Lung contusion.
'Crack' lung.
Arteriovenous malformation.
Aortic aneurysm.
Pulmonary embolism.
Mitral stenosis.
Other cause of pulmonary venous hypertension - eg, left ventricular failure.
Iatrogenic (eg, chest drain malposition, secondary to pulmonary artery catheter

Pulmonary endometriosis.
Congenital or acquired systemic coagulopathy - eg, leukaemia.
Anticoagulant or thrombolytic agents.
Factitious haemoptysis.

In most cases haemoptysis is a self-limiting event but in fewer than 5% it may be severe or
massive, representing a life-threatening condition that warrants urgent investigations and

Despite haemoptysis being regarded as an 'alarm' symptom, no identifiable cause is found in 15-
20% of cases and these are termed idiopathic or cryptogenic haemoptysis.

Haemoptysis is rare in children and often only presents where bleeding is substantial, as children
tend to swallow rather than expectorate their sputum. Respiratory tract infection is the most
common cause. Foreign body inhalation is the second most common cause (particularly with
younger children) and congenital heart disease and bronchiectasis secondary to cystic fibrosis are
other important causes.


Patients may find it hard to identify the origin of their bleeding.

Haemoptysis or haematemesis?
Haemoptysis Haematemesis
No nausea or vomiting Nausea and vomiting
Concurrent lung disease Concurrent gastric or hepatic disease
Sputum is frothy Vomitus is rarely frothy
Sputum has a liquid or clotted appearance Typical coffee ground appearance
Haemoptysis is bright red or pink Haematemesis is brown to black
Alkaline pH Acidic pH
Mixed with macrophages and neutrophils Mixed with food particles

Abrupt-onset cough, fever with bloody and purulent sputum - suggestive of acute
pneumonia or bronchitis.
Chronic productive cough - suggestive of chronic bronchitis or bronchiectasis.
Fevers, night sweats and weight loss - consider TB and other infections or malignancy.
Anorexia, weight loss and changing cough - think of possible bronchogenic carcinoma.
Dyspnoea, fatigue, orthopnoea, paroxysmal nocturnal dyspnoea, frothy pink sputum -
suggestive of congestive heart failure.
Dyspnoea and pleuritic chest pain - consider a PE.


Record vital signs, including oxygen saturation levels. Fever, tachycardia, tachypnoea, weight
loss and hypoxia are all relevant. Check for cachexia, cyanosis, pallor, ecchymoses,
telangiectasias and lymphadenopathy.

Inspect the nasal cavity and oropharynx for:

o Extrapulmonary causes (pseudohaemoptysis).
o Signs of vasculitis.

Gingival thickening, mulberry gingivitis, saddle nose, and nasal perforation suggest
Wegener's granulomatosis.

Perform a cardiovascular examination. Significant signs may include:

o The diastolic murmur of mitral stenosis.
o Signs of LVF.
o Tachypnoea, tachycardia, fixed split S2, pleural rub, and unilateral leg pain or
swelling which may indicate thromboembolic disease.
Lung signs that may be found with haemoptysis include:
o Fine inspiratory rales (associated with alveolar blood).
o Inspiratory and expiratory rhonchi (associated with airway secretions and blood).
Digital clubbing can reflect chronic lung disease
Supraclavicular lymphadenopathy, cachexia, hyperpigmentation, and Horner syndrome
may be associated with malignancy.

Major haemoptysis

This is a medical emergency with a high mortality rate. However, there are few large, good-
quality, controlled trials looking at best management to guide practice - particularly in the
medical versus surgical dilemma.

Resuscitate according to 'ABC' principles. Intubate where there are signs of acute
respiratory failure. Selective intubation of the right or left main bronchus with a large
single-lumen endotracheal tube or, alternatively, the use of a double lumen tube should be
considered. Maintain oxygenation saturations with high flow oxygen and suction. Obtain
IV access and give fluids/blood transfusion as appropriate. Correct any clotting
abnormalities. The patient will require admission to intensive care.
Localisation of the bleeding site via radiology and early bronchoscopy. CXR and even
CT scanning may not be helpful (due to the presence of aspirated blood). The use of rigid
or flexible fibreoptic bronchoscopy remains controversial and tends to depend on local
preference and expertise.
Specific therapies to control bleeding:
o Angiography and embolisation - endovascular embolisation is the most
effective and minimally invasive technique for managing massive and recurrent
o Bronchoscopic therapy:
Iced saline lavage.
Topical agents - eg, use of thrombin or fibrinogen-thrombin glue.
Endobronchial balloon catheter tamponade.
Laser photocoagulation.
o Surgical resection:

Under emergency conditions, surgery is difficult, has a high risk of septic

complications and a significant mortality rate. Surgery is usually only the
treatment of choice in selected cases, such as chest trauma and iatrogenic
pulmonary artery rupture. Emergency surgery should therefore be reserved for
patients with persistent life-threatening haemoptysis.

o Radiotherapy - may be used to treat aspergillomas and vascular tumours.

o Antifibrinolytic therapy - although there is currently insufficient evidence to
determine whether antifibrinolytics can be used to treat haemoptysis from any
cause, there is limited evidence to suggest they may reduce the duration of