COPD is commonly associated with progressive hypoxemia. Oxygen administration reduces mortality rates in patients with advanced COPD because of the favourable effects on pulmonary hemodynamics.

Long-term oxygen therapy improves survival 2-fold or more in hypoxemic patients with COPD, according to 2 landmark trials, the British Medical Research Council (MRC) study and the US National Heart, Lung and Blood Institute’s Nocturnal Oxygen Therapy Trial (NOTT). Hypoxemia is defined as PaO2 (partial pressure of oxygen in arterial blood) of less than 55 mm Hg or oxygen saturation of less than 90%. Oxygen was used for 15-19 hours per day.

Therefore, specialists recommend long-term oxygen therapy for patients with a PaO2 of less than 55 mm Hg, a PaO2 of less than 59 mm Hg with evidence of polycythaemia, or cor pulmonale. Patients should be evaluated after 1-3 months after initiating therapy, because some patients may not require long-term oxygen.

A history of measles, whooping cough, or other severe lung infections like tuberculosis (TB) and pneumonia can lead to airway damage and possibly bronchiectasis.

Paraneoplastic syndromes are more common in patients with lung cancer. Signs and symptoms include inappropriate antidiuretic hormone secretion, finger clubbing, hypercoagulability and Eaton-Lambert syndrome.

Pneumothorax refers to a condition in which air or gases accumulate inside the pleural space causing the lungs to collapse. Because the patient did not have a history of any previous pulmonary disease or trauma, this is a case of simple pneumothorax.

Hypogammaglobulinemia occurs due to a variety of underlying primary or secondary immunodeficient states, including HIV which is suspected in this case. The most commonly recognised clinical feature is recurrent infection.

A patient suffering from extrapulmonary restriction like a neuromuscular chest wall disorder would show similar signs and symptoms. Due to the restriction the lungs cannot fully inflate for gaseous exchange and hence TLCO drops. On the other hand, no change in cardiac output takes place and this leads to higher density of blood per unit volume resulting in raised KCO. No such findings are observed in diseases like scleroderma, PPH, hereditary haemorrhagic telangiectasia and alpha-1 antitrypsin deficiency.

A retrospective cohort study of the primary care records of 247 lung cancer patients diagnosed between 1998-2002 showed that 10% of the X-rays were reported as normal.
Other tests may include:
– Imaging tests: A CT scan can reveal small lesions in your lungs that might not be detected on an X-ray.
– Sputum cytology: sputum may reveal the presence of lung cancer cells.
– Tissue sample (biopsy): A sample of abnormal cells may be removed for histological analysis. A biopsy may be performed in a number of ways, including bronchoscopy, mediastinoscopy and needle biopsy. A biopsy sample may also be taken from adjacent lymph nodes.

Classic clinical features associated with active pulmonary TB are as follows (elderly individuals with TB may not display typical signs and symptoms):
– Cough
– Weight loss/anorexia
– Fever
– Night sweats
– Haemoptysis
– Chest pain (can also result from tuberculous acute pericarditis)
– Fatigue

Test:
Acid-fast bacilli (AFB) smear and culture – Using sputum obtained from the patient.
AFB stain is quick but requires a very high organism load for positivity, as well as the expertise to read the stained sample. This test is more useful in patients with pulmonary disease.
Obtain a chest radiograph to evaluate for possible associated pulmonary findings. If chest radiography findings suggest TB and a sputum smear is positive for AFB, initiate treatment for TB.

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:

Bird fancier’s lung (BFL) is a type of hypersensitivity pneumonitis (HP). It is triggered by exposure to avian proteins present in the dry dust of the droppings and sometimes in the feathers of a variety of birds. The lungs become inflamed, with granuloma formation. Birds such as pigeons, parakeets, cockatiels, shell parakeets (budgerigars), parrots, turtle doves, turkeys and chickens have been implicated.

People who work with birds or own many birds are at risk. Bird hobbyists and pet store workers may also be at risk. This disease is an inflammation of the alveoli in the lungs caused by an immune response to inhaled allergens from birds. Initial symptoms include shortness of breath (dyspnoea), especially after sudden exertion or when exposed to temperature change, which can resemble asthma, hyperventilation syndrome or pulmonary embolism. Chills, fever, non-productive cough and chest discomfort may also occur.

A definitive diagnosis can be difficult without invasive testing, but extensive exposure to birds combined with reduced diffusing capacity are strongly suggestive of this disease. X-ray or CT scans will show physical changes to the lung structure (a ground glass appearance) as the disease progresses. Precise distribution and types of tissue damage differ among similar diseases, as does response to treatment with Prednisone.

Serial Peak Expiratory Flow measurement at work and home is a feasible, sensitive, and specific test for the diagnosis of occupational asthma. For a diagnosis of occupational asthma, it is important to establish a relationship objectively between the workplace exposure and asthma symptoms and signs. Physiologically, this can be achieved by monitoring airflow limitation in relation to occupational exposure(s). If there is an effect of a specific workplace exposure, airflow limitation should be more prominent on work days compared with days away from work (or days away from the causative agent). Airflow limitation can be measured by spirometry, with peak expiratory flow (PEF) and/or forced expiratory volume in 1 s(FEV1) being the most useful for observing changes in airway calibre. Other tests mentioned are less reliable and would not help in establishing a satisfactory diagnosis of occupational asthma.

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.

Carbon monoxide (CO) is a colourless, odourless gas produced by incomplete combustion of carbonaceous material. Clinical presentation in patients with CO poisoning ranges from headache and dizziness to coma and death. Hyperbaric oxygen therapy can significantly reduce the morbidity of CO poisoning, but a portion of survivors still suffer significant long-term neurologic and affective sequelae.

Complaints:
Malaise, flulike symptoms, fatigue
Dyspnoea on exertion
Chest pain, palpitations
Lethargy
Confusion
Depression
Impulsiveness
Distractibility
Hallucination, confabulation
Agitation
Nausea, vomiting, diarrhoea
Abdominal pain
Headache, drowsiness
Dizziness, weakness, confusion
Visual disturbance, syncope, seizure
Faecal and urinary incontinence
Memory and gait disturbances
Bizarre neurologic symptoms, coma

Vital signs may include the following:
Tachycardia
Hypertension or hypotension
Hyperthermia
Marked tachypnoea (rare; severe intoxication often associated with mild or no tachypnoea)
Although so-called cherry-red skin has traditionally been considered a sign of CO poisoning, it is in fact rare.

The clinical diagnosis of acute carbon monoxide (CO) poisoning should be confirmed by demonstrating an elevated level of carboxyhaemoglobin (HbCO). Either arterial or venous blood can be used for testing. Analysis of HbCO requires direct spectrophotometric measurement in specific blood gas analysers. Elevated CO levels of at least 3-4% in non-smokers and at least 10% in smokers are significant.

Asthma patients have an increased risk of developing complications like pneumonia or collapsed lung. A clear visualization of the lungs through a CXR will define the management necessary for this patient.

Because of the patient’s acute presentation of symptoms accompanied by lung abnormalities observed on physical examination, the next step is to visualize the suspected acute inflammatory process by ordering a CXR. Bronchoscopy, CT and MRI are done in cases in which there is suspicion of any tumour formation. V/Q scan is done in cases where pulmonary embolism is suspected.

All of the symptoms observed in this patient are typical of bronchial carcinoma.

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.

Pulmonary surfactant is a mixture of lipids and proteins which is secreted by the epithelial type II cells into the alveolar space.

Tiotropium is a specific long-acting antimuscarinic agent indicated as maintenance therapy for patients with COPD (chronic obstructive pulmonary disease).
It should be used cautiously in patients with narrow-angle glaucoma, prostatic hyperplasia or bladder neck obstruction.
The most frequently encountered adverse effects of tiotropium include pharyngitis, bronchitis, sinusitis, dry mouth, cough, and headaches. Paradoxical bronchospasm may also occur as a rare side-effect.
Dry mouth occurs in up to 14% of patients taking tiotropium, in keeping with its anticholinergic profile.
Rarer side-effects include tachycardia, blurred vision, urinary retention, and constipation.

Non-invasive action via chest physiotherapy is helpful in the reduction or clearance of excessive secretions from airways.

Clinical criteria for the diagnosis of Buerger’s disease are:
1 – smoking history
2 – onset before the age of 50 years
3 – infrapopliteal arterial occlusions
4 – either upper limb involvement or phlebitis migrans
5 – absence of atherosclerotic risk factors other than smoking Confident clinical diagnosis of Buerger’s disease may be made only when all five requirements have been fulfilled.

Whilst asthma and COPD are different diseases they cause similar symptoms, which can present a challenge in identifying which of the two diseases a patient is suffering from. COPD causes chronic symptoms and narrowed airways which do not respond to treatment to open them up. In the case of asthma the constriction of the airways through inflammation tends to come and go and treatment to reduce inflammation and to open up the airways usually works well.

COPD is more likely than asthma to cause a chronic cough with phlegm and is rare before the age of 35 whilst asthma is common in under-35s. Disturbed sleep caused by breathlessness and wheeze is more likely in cases of asthma, as is a history of allergies, eczema and hay fever. Differentiating between COPD and asthma requires a history of both symptoms and spirometry. The spirometry history should include post bronchodilator measurements, the degree of reversibility and, ideally, home monitoring which gives a history of diurnal variation.

Airflow Obstruction: Both asthma and COPD are characterised by airflow obstruction. Airflow obstruction is defined as a reduced FEV1 and a reduced FEV1/FVC ratio, such that FEV1 is less than 80% of that predicted, and FEV1/FVC is less than 0.7.

These episodes are usually associated with widespread, but variable, airflow obstruction within the lung that is often reversible either spontaneously or with treatment.

COPD: COPD is a chronic, slowly progressive disorder characterised by airflow obstruction (reduced FEV1 and FEV1/VC ratio) that does not change markedly over several months. The airflow obstruction is not fully reversible.

Spirometry COPD Asthma
VC Reduced Nearly normal
FEV1 Reduced Reduced in attack
FVC (or FEV6) Reduced Nearly normal
FEV1 Ratio
(of VC/FVC/FEV6) Reduced in attack

This man has a low FEV1 and FVC. His diffusions capacity is also low despite having a normal total lung capacity. These values confirm a diagnosis of COPD.

Sarcoidosis is a chronic inflammatory condition that can affect any organ but mainly affects the lungs and lymph nodes. Cough can be due to any of the given conditions. Polyarthritis, erythema nodosum (erythematous painful subcutaneous nodules) and symmetric hilar and mediastinal lymphadenopathy are classical signs of sarcoidosis. This triad is known as Lofgren syndrome.

Prolonged compression of the trachea by a large goitre will cause tracheomalacia following thyroidectomy.

Small cell lung cancer (SCLC) is characterized by rapid growth and early dissemination. Prompt initiation of treatment is important.

Patients with clinical stage Ia (T1N0) after standard staging evaluation may be considered for surgical resection, but combined treatment with chemotherapy and radiation therapy is the standard of care. Radiation therapy is often added at the second cycle of chemotherapy.

Historically, patients undergoing surgery for small cell lung cancer (SCLC) had a dismal prognosis. However, more recent data suggest that patients with true stage I SCLC may benefit from surgical resection.

Common sites of hematogenous metastases include the brain, bones, liver, adrenal glands, and bone marrow. The symptoms depend upon the site of spread.

Sarcoidosis is an inflammatory disease that affects one or more organs but most commonly affects the lungs and lymph glands. The inflammation may change the normal structure and possibly the function of the affected organ(s).
The presentation in sarcoidosis varies with the extent and severity of organ involvement, as follows:
Asymptomatic (incidentally detected on chest imaging): Approximately 5% of cases.
Systemic complaints (fever, anorexia): 45% of cases
Pulmonary complaints (dyspnoea on exertion, cough, chest pain, and haemoptysis [rare]): 50% of cases

Löfgren syndrome (fever, bilateral hilar lymphadenopathy, and polyarthralgias): Common in Scandinavian patients, but uncommon in African-American and Japanese patients.

Dermatologic manifestations may include the following:
– Erythema nodosum
– A lower-extremity panniculitis with painful, erythematous nodules (often with Löfgren syndrome)
– Lupus pernio (the most specific associated cutaneous lesion)
– Violaceous rash on the cheeks or nose (common)
– Maculopapular plaques (uncommon)

Staging of sarcoidosis is as follows:
Stage 0: Normal chest radiographic findings
Stage I: Bilateral hilar lymphadenopathy
Stage II: Bilateral hilar lymphadenopathy and infiltrates
Stage III: Infiltrates alone
Stage IV: Fibrosis

Nonsteroidal anti-inflammatory drugs (NSAIDs) are indicated for the treatment of arthralgias and other rheumatic complaints. Patients with stage I sarcoidosis often require only occasional treatment with NSAIDs.

Treatment in patients with pulmonary involvement is as follows:
Asymptomatic patients may not require treatment
In patients with minimal symptoms, serial re-evaluation is prudent
Treatment is indicated for patients with significant respiratory symptoms
Corticosteroids can produce small improvements in the functional vital capacity and in the radiographic appearance in patients with more severe stage II and III disease.

This patient has Stage 1 Sarcoidosis so observation is the most appropriate action.

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.

A drop in level of consciousness is an indicator of high levels of PCO2 and cerebral cortex depression. It is a life threatening condition that requires intervention which may include mechanical ventilation.

Cavitating pneumonia is a complication that can occur with a severe necrotizing pneumonia and in some publications it is used synonymously with the latter term. It is a rare complication in both children and adults. Albeit rare, cavitation is most commonly caused by Streptococcus pneumoniae, and less frequently Aspergillus spp., Legionella spp. and Staphylococcus aureus.

In children, cavitation is associated with severe illness, although cases usually resolve without surgical intervention, and long-term follow-up radiography shows clear lungs without pulmonary sequelae
Although the absolute cavitary rate may not be known, according to one series, necrotizing changes were seen in up to 6.6% of adults with pneumococcal pneumonia. Klebsiella pneumoniae is another organism that is known to cause cavitation.

Causative agents:
Mycobacterium tuberculosis
Klebsiella pneumoniae
Streptococcus pneumoniae
Staphylococcus aureus

Enterococcus faecalis was not found to be a causative agent.

Silicosis is a common occupational lung disease that is caused by the inhalation of crystalline silica dust. Silica is the most abundant mineral on earth. Workers that are involved for example in construction, mining, or glass production are among the individuals with the highest risk of developing the condition. Acute silicosis causes severe symptoms (e.g., exertional dyspnoea, cough with sputum) and has a very poor prognosis.
Chronic silicosis has a very variable prognosis and affected individuals may remain asymptomatic for several decades. However, radiographic signs are usually seen early on. Typical radiographic findings are calcifications of perihilar lymph nodes, diffuse ground glass opacities, large numbers of rounded, solitary nodules or bigger, confluent opacities. Avoiding further exposure to silica is crucial, especially since the only treatment available is symptomatic (e.g., bronchodilators). Silicosis is associated with an increased risk of tuberculosis and lung cancer. Berylliosis typically affects individuals who are exposed to aerospace industry. Histoplasmosis and tuberculosis do not form eggshell calcifications.