Assess the need for oxygen therapy in people with:
– very severe airflow obstruction (FEV1 below 30% predicted)
– cyanosis (blue tint to skin)
– polycythaemia
– peripheral oedema (swelling)
– a raised jugular venous pressure
– oxygen saturations of 92% or less breathing air.

Also consider assessment for people with severe airflow obstruction (FEV1 30–49% predicted).

Consider long-term oxygen therapy for people with COPD who do not smoke and who:
have a partial pressure of oxygen in arterial blood (PaO2) below 7.3 kPa when stable or have a PaO2 above 7.3 and below 8 kPa when stable, if they also have 1 or more of the following:
– secondary polycythaemia
– peripheral oedema
– pulmonary hypertension.

Smoking cessation is the most effective intervention in stopping the progression of COPD, as well as increasing survival and reducing morbidity. This is why smoking cessation should be the top priority in the treatment of COPD. Long term oxygen therapy (LTOT) may increase survival in hypoxic patients. The rest of the options dilate airways, reduce inflammation and thereby improve symptoms but do not necessarily increase survival.

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.

Squamous-cell carcinoma is the most common histological type of lung cancer to cavitate (82% of cavitary primary lung cancer), followed by adenocarcinoma and large cell carcinoma. Multiple cavitary lesions in primary lung cancer are rare, however, multifocal bronchoalveolar cell carcinoma can occasionally have multiple cavitary lesions. Small cell carcinoma is not known to cavitate.

Lambert-Eaton myasthenic syndrome (LEMS) is a rare presynaptic disorder of neuromuscular transmission in which release of acetylcholine (ACh) is impaired, causing a unique set of clinical characteristics, which include proximal muscle weakness, depressed tendon reflexes, post-tetanic potentiation, and autonomic changes.

In 40% of patients with LEMS, cancer is present when the weakness begins or is found later. This is usually a small cell lung cancer (SCLC). However, LEMS has also been associated with non-SCLC, lymphosarcoma, malignant thymoma, or carcinoma of the breast, stomach, colon, prostate, bladder, kidney, or gallbladder.

Caplan’s syndrome is defined as the association between silicosis and rheumatoid arthritis (RA). It is rare and usually diagnosed in an advanced stage of RA. It generally affects patients with a prolonged exposure to silica.

Caplan’s syndrome presents with rheumatoid lung nodules and pneumoconiosis. Originally described in coal miners with progressive massive fibrosis, it may also occur in asbestosis, silicosis and other pneumoconiosis. Chest radiology shows multiple, round, well defined nodules, usually 0.5 – 2.0 cm in diameter, which may cavitate and resemble tuberculosis.

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.

Community-acquired pneumonia (CAP) is one of the most common infectious diseases and is an important cause of mortality and morbidity worldwide. Typical bacterial pathogens that cause CAP include Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis.
The CURB-65 is used as a means of deciding the action that is needed to be taken for that patient.
Score 3-5: Requires hospitalization with consideration as to whether they need to be in the intensive care unit

Recent studies have suggested that the use of a beta-lactam alone may be noninferior to a beta-lactam/macrolide combination or fluoroquinolone therapy in hospitalized patients.

Therapy in ICU patients includes the following:
– Beta-lactam (ceftriaxone, cefotaxime, or ampicillin/sulbactam) plus either a macrolide or respiratory fluoroquinolone
– For patients with penicillin allergy, a respiratory fluoroquinolone and aztreonam

Therefore the appropriate treatment would be Cefotaxime and erythromycin.

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.

The normal partial pressure reference values are:
– PaO2 more than 80 mmHg (11 kPa)
– PaCO2 less than 45 mmHg (6.0 kPa).
This patient has an elevated PaCO2 (7.4kPa)
Hypoxemia (PaO2 <8kPa) with hypercapnia (PaCO2 >6.0kPa).
The pH is also lower than 7.35 at 7.3

Type 2 respiratory failure is caused by inadequate alveolar ventilation; both oxygen and carbon dioxide are affected. Defined as the build-up of carbon dioxide levels (PaCO2) that has been generated by the body but cannot be eliminated. The underlying causes include:
– Increased airways resistance (chronic obstructive pulmonary disease, asthma, suffocation)
– Reduced breathing effort (drug effects, brain stem lesion, extreme obesity)
– A decrease in the area of the lung available for gas exchange (such as in chronic bronchitis)
– Neuromuscular problems (Guillain–Barré syndrome, motor neuron disease)
– Deformed (kyphoscoliosis), rigid (ankylosing spondylitis), or flail chest.

CURB Pneumonia Severity Score estimates the mortality of community-acquired pneumonia to help determine inpatient vs. outpatient treatment.
Select Criteria:
Confusion (abbreviated Mental Test Score <=8) (1 point)
Urea (BUN > 19 mg/dL or 7 mmol/L) (1 point)
Respiratory Rate > 30 per minute (1 point)
Blood Pressure: diastolic < 60 or systolic < 90 mmHg (1 point) The CURB-65 scores range from 0 to 5. Clinical management decisions can be made based on the score:
Score Risk Disposition
0 or 1 – 1.5% mortality – Outpatient care
2 – 9.2% mortality – Inpatient vs. observation admission
≥ 3 – 22% mortality – Inpatient admission with consideration for ICU admission with score of 4 or 5

High-resolution CT (HRCT) scanning is more sensitive than standard chest radiography and is highly specific for diagnosing emphysema (outlined bullae are not always visible on a radiograph).

HRCT scanning may provide an adjunct means of diagnosing various forms of COPD (i.e., lower lobe disease may suggest AAT deficiency) and may help the clinician to determine whether surgical intervention would benefit the patient.

The phrenic nerve provides the primary motor supply to the diaphragm, the major respiratory muscle.
Phrenic nerve paralysis is a rare cause of exertional dyspnoea that should be included in the differential diagnosis. Fluoroscopy is considered the most reliable way to document diaphragmatic paralysis. During fluoroscopy a patient is asked to sniff and there is a paradoxical rise of the paralysed hemidiaphragm. This is to confirm that the cause is due to paralysis rather than unilateral weakness.

Allergic bronchopulmonary aspergillosis (ABPA) is a form of lung disease that occurs in some people who are allergic to Aspergillus. With ABPA, this allergic reaction causes the immune system to overreact to Aspergillus leading to lung inflammation. ABPA causes bronchospasm (tightening of airway muscles) and mucus build-up resulting in coughing, breathing difficulty and airway obstruction.

Blood tests are used to look for signs of an allergic reaction. This includes evaluating your immunoglobulin E (IgE) level. This level is increased with any type of allergy. Many people with asthma have higher than normal IgE levels. In ABPA however, the IgE level is extremely high (more than 1000 ng/ml or 417 IU/ml). In addition to total IgE, all patients with ABPA have high levels of IgE that is specific to Aspergillus. A blood test can be done to measure specific IgE to Aspergillus. A blood or skin test for IgE antibodies to Aspergillus can be done to see if a person is sensitized (allergic) to this fungus. If these skin tests are negative (i.e. does not show a skin reaction) to Aspergillus fumigatus, the person usually does not have ABPA.
Therefore, there should be no change in medication since this patient does not have ABPA.

Postmenopausal oestrogen therapy and hormone therapy are associated with an increased risk of thromboembolism. The relative risk seems to be even greater if the treated population has pre-existing risk factors for thromboembolism, such as obesity, immobilization, and fracture. Cor pulmonale can occur secondary to small recurrent pulmonary embolisms. Pneumonias and bronchiectasis usually present with purulent sputum, and in case of carcinoma there may be other associated symptoms like weight loss, etc.

Pneumothorax is defined as air in the pleural space and may be classified as spontaneous, traumatic or iatrogenic. Primary spontaneous pneumothorax occurs in patients without clinically apparent lung disease.
Primary pneumothorax has an incidence of 18-28 per 100,000 per year for men and 1.2-6 per 100,000 per year for women. Most patients present with ipsilateral pleuritic chest pain and acute shortness of breath. Shortness of breath is largely dependent on the size of the pneumothorax and whether there is underlying chronic lung disease.

Young patients may have chest pain only. Most episodes of pneumothorax occur at rest. Symptoms may resolve within 24 hours in patients with primary spontaneous pneumothorax. The diagnosis of a pneumothorax is confirmed by finding a visceral pleural line displaced from the chest wall, without distal lung markings, on a posterior-anterior chest radiograph.

Breathless patients should not be left without intervention regardless of the size of pneumothorax. If there is a rim of air >2cm on the chest X-ray, this should be aspirated.
Aspiration is successful in approximately 70 per cent of patients; the patient may be discharged subsequently. A further attempt at aspiration is recommended if the patient remains symptomatic and a volume of less than 2.5 litres has been aspirated on the first attempt.

If unsuccessful, an intercostal drain is inserted. This may be removed after 24 hours after full re-expansion or cessation of air leak without clamping and discharge may be considered.

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.

The following drugs should be used as normal during pregnancy:
short acting β2 -agonists
long acting β2- agonists
inhaled corticosteroids
oral and intravenous theophyllines

Use steroid tablets as normal when indicated during pregnancy for severe asthma. Steroid tablets should never be withheld because of pregnancy.
If leukotriene receptor antagonists are required to achieve adequate control of asthma then they should not be withheld during pregnancy.

V/Q scanning carries a slightly increased risk of childhood cancer compared with CTPA – 1/280,000 versus less than 1/1,000,000 – but carries a lower risk of maternal breast cancer. The rest of the options are true.

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.

Severe acute respiratory syndrome (SARS) is a viral respiratory illness caused by a coronavirus called SARS-associated coronavirus (SARS-CoV). SARS was first reported in Asia in February 2003.
In general, SARS begins with a high fever (temperature greater than 38.0°C). Other symptoms may include headache, an overall feeling of discomfort, and body aches. Some people also have mild respiratory symptoms at the outset. About 10 to 20 percent of patients have diarrhoea. After 2 to 7 days, SARS patients may develop a dry cough. Most patients develop pneumonia. 

Lofgren’s syndrome is an acute form of sarcoidosis characterized by erythema nodosum, bilateral hilar lymphadenopathy (BHL), and polyarthralgia or polyarthritis. Other symptoms include anterior uveitis, fever, ankle periarthritis, and pulmonary involvement.

Löfgren syndrome is usually an acute disease with an excellent prognosis, typically resolving spontaneously from 6-8 weeks to up to 2 years after onset. Pulmonologists, ophthalmologists, and rheumatologists often define this syndrome differently, describing varying combinations of arthritis, arthralgia, uveitis, erythema nodosum, hilar adenopathy, and/or other clinical findings.

Long-term oxygen therapy (LTOT) ≥ 15 h/day improves survival in hypoxemic chronic obstructive pulmonary disease (COPD). It significantly helps in reducing pulmonary hypertension associated with COPD and treating underlying pathology of future heart failure. There is little to no benefit of oxygen therapy for less than 15 hours.

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 vas deferens is a long tube that connects the epididymis to the ejaculatory ducts. It acts as a canal through which mature sperm may pass through the penis during ejaculation.

Most men with CF (97-98 percent) are infertile because of a blockage or absence of the vas deferens, known as congenital bilateral absence of the vas deferens (CBAVD). The sperm never makes it into the semen, making it impossible for them to reach and fertilize an egg through intercourse. The absence of sperm in the semen can also contribute to men with CF having thinner ejaculate and lower semen volume.

Pulmonary alveolar proteinosis (PAP) is a lung condition that is caused by a build-up of proteins and other substances in the alveoli. The alveoli are the part of the lungs that contain air. PAP has the following symptoms:
Shortness of breath, also called dyspnoea
Chest pain or tightness
Fever
Weight loss
Cough (sometimes, but not always)
Low levels of oxygen in the blood
Nail clubbing (abnormal growth of toenails or fingernails)

Serologic studies are generally not useful for PAP. Flexible bronchoscopy with bronchoalveolar lavage (BAL) remains the criterion standard. Elevated levels of the proteins SP-A and SP-D in serum and BAL fluid may be useful. Elevated titer of neutralizing autoantibody against GM-CSF (immunoglobulin G [IgG] isotype) in serum and BAL fluid may be useful. Recent studies have proposed that deficiency of GM-CSF causes pulmonary alveolar proteinosis (PAP); all patients studied had the antibody to GM-CSF. Serum lactate dehydrogenase (LDH) level is usually elevated, but this finding is nonspecific.

High-resolution computed tomography (HRCT) scan of the chest demonstrates areas of patchy ground-glass opacification with smooth interlobular septal thickening and intralobular interstitial thickening, which produces a polygonal pattern referred to as crazy paving.

Light microscopy of the lung parenchymal tissue shows alveoli filled with a granular PAS base-reactive and diastase-resistant eosinophilic material.

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.

Cystic fibrosis (CF) is a multisystemic, autosomal recessive disorder that predominantly affects infants, children, and young adults. CF is the most common life-limiting genetic disorder in whites, with an incidence of 1 case per 3200-3300 new-borns in the United States.

People with CF can have a variety of symptoms, including:
Very salty-tasting skin
Persistent coughing, at times with phlegm
Frequent lung infections including pneumonia or bronchitis
Wheezing or shortness of breath
Poor growth or weight gain in spite of a good appetite
Frequent greasy, bulky stools or difficulty with bowel movements
Male infertility

Signs of bronchiectasis include the tubular shadows; tram tracks, or horizontally oriented bronchi; and the signet-ring sign, which is a vertically oriented bronchus with a luminal airway diameter that is 1.5 times the diameter of the adjacent pulmonary arterial branch.

Bronchiectasis is characterized by parallel, thick, line markings radiating from hila (line tracks) in cylindrical bronchiectasis. Ring shadows represent dilated thick-wall bronchi seen in longitudinal section or on-end or dilated bronchi in varicose bronchiectasis.

Pseudomonas aeruginosa is the key bacterial agent of cystic fibrosis (CF) lung infections, and the most important pathogen in progressive and severe CF lung disease. This opportunistic pathogen can grow and proliferate in patients, and exposure can occur in hospitals and other healthcare settings.

Haemophilus influenzae is regularly involved in chronic lung infections and acute exacerbations of CF patients

In mild-to-moderate heroin overdoses, arterial blood gas (ABG) analysis reveals respiratory acidosis. In more severe overdoses, tissue hypoxia is common, leading to mixed respiratory and metabolic acidosis.

The normal range for PaCO2 is 35-45 mmHg (4.67 to 5.99 kPa). Respiratory acidosis can be acute or chronic. In acute respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range (i.e., >45 mm Hg) with an accompanying academia (i.e., pH < 7.35). In chronic respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range, with a normal or near-normal pH secondary to renal compensation and an elevated serum bicarbonate levels (i.e., >30 mEq/L).

Arterial blood gases with pH = 7.31; pCO2 = 7.4 kPa; pO2 = 8.1 kPa would indicate respiratory acidosis.

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.