Extrinsic allergic alveolitis (EAA) refers to a group of lung diseases that can develop after exposure to certain substances. The name describes the origin and the nature of these diseases:

‘extrinsic’ – caused by something originating outside the body
‘allergic’ – an abnormally increased (hypersensitive) body reaction to a common substance
‘alveolitis’ – inflammation in the small air sacs of the lungs (alveoli)

Symptoms can include: fever, cough, worsening breathlessness and weight loss. The diagnosis of the disease is based on a history of symptoms after exposure to the allergen and a range of clinical tests which usually includes: X-rays or CT scans, lung function and blood tests.

EAA is not a ‘new’ occupational respiratory disease and occupational causes include bacteria, fungi, animal proteins, plants and chemicals.

Examples of EAA include:

Farmer’s lung
This is probably the most common occupational form of EAA and is the outcome of an allergic response to a group of microbes, which form mould on vegetable matter in storage. During the handling of mouldy straw, hay or grain, particularly in a confined space such as a poorly ventilated building, inhalation of spores and other antigenic material is very likely.

There also appears to be a clear relationship between water content of crops, heating (through mould production) and microbial growth, and this would apply to various crops and vegetable matter, with the spores produced likely to cause EAA.

Farmer’s lung can be prevented by drying crops adequately before storage and by ensuring good ventilation during storage. Respiratory protection should also be worn by farm workers when handling stored crops, particularly if they have been stored damp or are likely to be mouldy.

Occupational asthma (OA) could be divided into a nonimmunological, irritant-induced asthma and an immunological, allergy-induced asthma. In addition, allergy-induced asthma can be caused by two different groups of agents: high molecular weight proteins (>5,000 Da) or low molecular weight agents (<5,000 Da), generally chemicals like the isocyanates.
Isocyanates are very reactive chemicals characterized by one or more isocyanate groups (–N=C=O). The main reactions of this chemical group are addition reactions with ethanol, resulting in urethanes, with amines (resulting in urea derivates) and with water. Here, the product is carbamic acid which is not stable and reacts further to amines, releasing free carbon dioxide.

Diisocyanates and polyisocyanates are, together with the largely nontoxic polyol group, the basic building blocks of the polyurethane (PU) chemical industry, where they are used solely or in combination with solvents or additives in the production of adhesives, foams, elastomers, paintings, coatings and other materials.

The complex salts of platinum are one of the most potent respiratory sensitising agents having caused occupational asthma in more than 50% of exposed workers. Substitution of ammonium hexachlor platinate with platinum tetra amine dichloride in the manufacture of catalyst has controlled the problem in the catalyst industry. Ammonium hexachlorplatinate exposure still occurs in the refining process.

Rosin based solder flux fume is produced when soldering. This fume is a top cause of occupational asthma.

Bakeries, flour mills and kitchens where flour dust and additives in the flour are a common cause of occupational asthma.

Cadmium was not found to cause occupational asthma.

Bronchial carcinoids are uncommon, slow growing, low-grade, malignant neoplasms, comprising 1-2% of all primary lung cancers.
It is believed to be derived from surface of bronchial glandular epithelium. Mostly located centrally, they produce symptoms and signs of bronchial obstruction such as localized wheeze, non resolving recurrent pneumonitis, cough, chest pain, and fever. Haemoptysis is present in approximately 50% of the cases due to their central origin and hypervascularity.
Central bronchial carcinoids are more common than the peripheral type and are seen as endobronchial nodules or hilar/perihilar mass closely related to the adjacent bronchus. Chest X-ray may not show the central lesion depending on how small it is.

The tumour has only invaded the visceral pleura and measures 3cm in the greatest dimension. Hence it is designated at T2. Ipsilateral peribronchial and/or hilar lymph node involvement would make it N1. There is no distal metastasis so M would be 0.

Acute epiglottitis is a life-threatening disorder with serious implications to the anaesthesiologist because of the potential for laryngospasm and irrevocable loss of the airway. There is inflammatory oedema of the arytenoids, aryepiglottic folds and the epiglottis; therefore, supraglottitis may be used instead or preferred to the term acute epiglottitis.

Acute epiglottitis can occur at any age. The responsible organism used to be Hemophilus influenzae type B (Hib), but infection with group A b-haemolytic Streptococci has become more frequent after the widespread use of Hemophilus influenzae vaccination.

The typical presentation in epiglottitis includes acute occurrence of high fever, severe sore throat and difficulty in swallowing with the sitting up and leaning forward position in order to enhance airflow. There is usually drooling because of difficulty and pain on swallowing. Acute epiglottitis usually leads to generalized toxaemia. The most common differential diagnosis is croup and a foreign body in the airway. A late referral to an acute care setting with its serious consequences may result from difficulty in differentiation between acute epiglottitis and less urgent causes of a sore throat, shortness of breath and dysphagia.

The right and left lung anatomy are similar but asymmetrical. The right lung consists of three lobes: right upper lobe (RUL), right middle lobe (RML), and right lower lobe (RLL). The left lung consists of two lobes: right upper lobe (RUL) and right lower lobe (RLL). The right lobe is divided by an oblique and horizontal fissure, where the horizontal fissure divides the upper and middle lobe, and the oblique fissure divides the middle and lower lobes. In the left lobe there is only an oblique fissure that separates the upper and lower lobe.

The lobes further divide into segments which are associated with specific segmental bronchi. Segmental bronchi are the third-order branches off the second-order branches (lobar bronchi) that come off the main bronchus.

The right lung consists of ten segments. There are three segments in the RUL (apical, anterior and posterior), two in the RML (medial and lateral), and five in the RLL (superior, medial, anterior, lateral, and posterior). The oblique fissure separates the RUL from the RML, and the horizontal fissure separates the RLL from the RML and RUL.

There are eight to nine segments on the left depending on the division of the lobe. In general, there are four segments in the left upper lobe (anterior, apicoposterior, inferior and superior lingula) and four or five in the left lower lobe (lateral, anteromedial, superior and posterior). The medium sized airways offer the maximum airway resistance, not smaller ones.

Bronchopneumonia presents as a patchy consolidation involving one or more lobes, usually the dependent lung zones, a pattern attributable to aspiration of oropharyngeal contents.

Symptoms of bronchopneumonia may be like other types of pneumonia. This condition often begins with flu-like symptoms that can become more severe over a few days. The symptoms include:
– fever
– a cough that brings up mucus
– shortness of breath
– chest pain
– rapid breathing
– sweating
– chills
– headaches
– muscle aches
– pleurisy, or chest pain that results from inflammation due to excessive coughing
– fatigue
– confusion or delirium, especially in older people

There are several factors that can increase your risk of developing bronchopneumonia. These include:
– Age: People who are 65 years of age or older, and children who are 2 years or younger, have a higher risk for developing bronchopneumonia and complications from the condition.
– Environmental: People who work in, or often visit, hospital or nursing home facilities have a higher risk for developing bronchopneumonia.
– Lifestyle: Smoking, poor nutrition, and a history of heavy alcohol use can increase your risk for bronchopneumonia.
– Medical conditions: Having certain medical conditions can increase your risk for developing this type of pneumonia. These include: chronic lung disease, such as asthma or chronic obstructive pulmonary disease (COPD), HIV/AIDS, having a weakened immune system due to chemotherapy or the use of immunosuppressive drugs.

Phrenic nerve palsy causing hemidiaphragm paralysis is a very uncommon feature of thoracic aortic aneurysm.

Thoracic aortic aneurysms are usually asymptomatic however chest pain is most commonly reported symptom. Left hemidiaphragm paralysis, because of left phrenic nerve palsy, is a very rare presentation of thoracic aortic aneurysm.
Thoracic aortic aneurysm may present atypical symptoms such as dysphagia due to compression of the oesophagus; hoarseness due to vocal cord paralysis or compression of the recurrent laryngeal nerve; superior vena cava syndrome due to compression of the superior vena cava; cough, dyspnoea or both due to tracheal compression; haemoptysis due to rupture of the aneurysm into a bronchus; and shock due to rupture of the aneurysm.
Common causes of phrenic nerve palsy include malignancy such as bronchogenic carcinoma, as well as mediastinal and neck tumours. Phrenic nerve palsy can also occur due to a penetrating injury or due to iatrogenic causes arising, for example, during cardiac surgery and central venous catheterization. Many cases or phrenic nerve palsy are idiopathic.

High Altitude Cerebral Oedema (HACE) is a severe and potentially fatal manifestation of high altitude illness and is often characterized by ataxia, fatigue, and altered mental status. HACE is often thought of as an extreme form/end-stage of Acute Mountain Sickness (AMS). Although HACE represents the least common form of altitude illness, it may progress rapidly to coma and death as a result of brain herniation within 24 hours, if not promptly diagnosed and treated.

HACE generally occurs after 2 days above 4000m but can occur at lower elevations (2500m) and with faster onset. Some, but not all, individuals will suffer from symptoms of AMS such as headache, insomnia, anorexia, nausea prior to transitioning to HACE. Some may also have concomitant High Altitude Pulmonary Oedema (HAPE). HACE in isolation is rare, but the absence of concomitant HAPE or symptoms of AMS prior to deterioration does not rule-out the presence of HACE.

Most cases develop as a progression of AMS and will include a history of recent ascent to altitude and prior complaints/findings of AMS including a headache, fatigue, nausea, insomnia, and/or light-headedness. Some may also have signs/symptoms of HAPE. Transition to HACE is heralded by signs of encephalopathy including ataxia (usually the earliest clinical finding) and altered mentation which may range from mild to severe. Other symptoms may include a more severe headache, difficulty speaking, lassitude, a decline in the level of consciousness, and/or focal neurological deficits or seizures.

The mainstay of treatment is the immediate descent of at least 1000m or until symptoms improve. If descent is not an option, one may use a portable hyperbaric chamber and/or supplemental oxygen to temporize illness, but this should never replace or delay evaluation/descent when possible. If available, dexamethasone 8mg for one dose, followed by 4mg every 6 hours should be given to adults via PO, IM, or IV routes.
Acetazolamide has proven to be beneficial in only a single clinical study. The suggested dosing regimen for Acetazolamide is 250 mg PO, given twice daily. Though effective in alleviating or temporizing symptoms, none of the adjunct treatment modalities are definitive or a replacement for an immediate descent.

Bronchiectasis is a long-term condition where the airways of the lungs become abnormally widened, leading to a build-up of excess mucus that can make the lungs more vulnerable to infection. The most common symptoms of bronchiectasis include:
– a persistent productive cough
– breathlessness.

The 3 most common causes in the UK are:
– a lung infection in the past, such as pneumonia or whooping cough, that damages the bronchi
– underlying problems with the immune system (the body’s defence against infection) that make the bronchi more vulnerable to damage from an infection
– allergic bronchopulmonary aspergillosis (ABPA) – an allergy to a certain type of fungi that can cause the bronchi to become inflamed if spores from the fungi are inhaled