frequency of exacerbations.Respiratory medicine: overview
Respiratory medicine: in clinic
Respiratory medicine is a medical speciality dealing with disorders of the respiratory system. The predominant population are patients with chronic lung disease often related to smoking.
Such patients are not hard to find—in fact they can be found almost everywhere. These patients are usually managed by their GP in the community, but may be referred to clinic if difficult to treat and for frequency of exacerbations.
Much like COPD, asthmatic patients can be found almost anywhere. While most are managed by the GP in the community, patients with more severe asthma can be followed up in clinic. You may also see acute asthma attacks and refractory cases presenting to ED who will need at least admission if not further intervention such as intubation.
Lung cancer is managed by a MDT so you may find it more useful to attend thoracic clinics to learn about the non-operative and operative interventions offered by the oncologists and surgeons respectively.
These patients are distinctively shared by the respiratory team as well as an immunologist to identify their triggers. You will find these patients in clinic with long-term follow-up.
This is becoming an increasingly common problem due to obesity rates in developed countries. You can find these patients in respiratory clinic with consultations with bariatric surgeons and sleep study suites.
You can find these patients in clinic as long-term follow-up. This disease is commoner in adults including those with recurrent pneumonia, autoimmunity, and extraintestinal features of IBD. Children with cystic fibrosis and those immunocompromised (e.g. AIDS 
recurrent pneumonia destruction of elastic tissue scarring) are also susceptible.
Patients are going to be children and adolescents followed up both in the community and the clinic. Since most patients are children, most exacerbations will be admitted onto paediatric ward. Extrapulmonary manifestations (e.g. endocrine, GI, subfertility) are also followed up in respective outpatients.
There are two types: type 1 (hypoxic and known as ‘pink puffers’) and type 2 (hypoxic and hypercapnic also known as ‘blue bloaters’). Patients with chronic failure are managed by the GP but are also followed up in clinics with specialist respiratory nurses and physicians. Acute exacerbations present to ED where patient ought to be thoroughly investigated for reversible causes.
Depending on the extent of dyspnoea, pyrexia, and dehydration, patients may require admission for IV antibiotics and hydration especially if there is another respiratory comorbidity such as asthma or COPD. Otherwise, community-acquired pneumonias are frequently treated in the community.
You will see patients (children with asthma and adults with COPD who smoke) with acute dyspnoea from either infective or non-infective causes who almost always require at least monitoring on the wards for a few days if not antibiotics and steroids. Refractory asthma attacks (status asthmaticus) is a medical emergency and may need sedation, intubation and ventilation on the ITU.
This is a medical emergency in which not only does the treatment need to commence immediately, but any underlying disease or reversible causes need to be addressed to prevent further propagation of clots. Patients will present with dyspnoea, pleuritic chest pain, and possibly haemoptysis.
You will encounter patients with dyspnoea, a wet persistent cough, and fluid overload who cannot manage their symptoms with oral medication (e.g. diuretics) at home. The underlying cause is often cardiac and/or renal failure or hypoalbuminaemia. Patients need to be admitted for offloading and (sometimes invasive) monitoring.
Moderately sized effusions will present as severity of dyspnoea. As well as treatment, the underlying disease/cause ought to be investigated and treated. Beware of chylothorax (lymph fluid) or haemothorax (blood) in trauma patients with penetrating injuries (e.g. stab).
Leakage of air into the pleuritic space can be disastrous! Tension pneumothorax where the mediastinum and trachea shift away is a medical emergency. May either be primary (spontaneous) or due to trauma (e.g. penetrating injury).
These are ubiquitous in any speciality and you will undoubtedly be expected to present them at ward rounds and in clinics.
You will be able to attend theatre lists of bronchoscopy conducted either by the respiratory or the cardiothoracic teams. You will be expected to know about the procedure, its indications, contraindications, and complications, to consent a patient confidently in your exams.
You will be able to see these inserted on the ward for stable patients or in a resuscitation bay for trauma patients with haemo/pneumothorax.
Pleurocentesis is a procedure that can save lives but it is important to understand the key anatomical landmarks for doing one to avoid iatrogenic injury. These often be seen in a resuscitation bay with tension pneumothorax. Fluid aspirations diagnose content of pleural effusions.
This is also known as pulmonary function tests and depicts spirograms of flow (litres per second) against volume. Flow–volume loops may also be another option. Differences in loop shapes are observed between restrictive and obstructive pulmonary diseases as well as acute obstruction. This investigation is usually conducted in the outpatient clinic. (See Fig. 30.1.)
Fig. 30.1 Spirometry. Reproduced with permission from Wilkinson, Ian, et al, Oxford Handbook of Clinical Medicine 10e, 2017: Oxford University Press.
Rule out pulmonary embolus. CTPA may be contraindicated in pregnancy in which the older V/Q scan modality is suitable. You can also discuss which modality is optimal in various clinical scenarios.
Is usually seen on either the respiratory ward or HDU/ITU.
In refractory cases of pleural effusions, obliterating the pleural space with tetracycline, bleomycin, or talcum powder.
Lung disease causing shortness of breath is classified into obstructive or restrictive disease, strictly based on spirometry.
Most commonly asthma and COPD (forced expiratory volume in 1 sec (FEV1)/FVC <0.8, FEV1 <80% predicted) causing reduced airflow due to bronchoconstriction or obstruction (mucosal inflammation and mucus).
Intrinsic lung fibrosis (most commonly interstitial pulmonary fibrosis) or extrinsic chest wall disease (e.g. myasthenia gravis, Guillain–Barré; FEV1/FVC >0.8) leads to a chest which is difficult to expand.
Is typified by reversibility of airway obstruction, diurnal variation in symptoms/PEFR (worse in mornings), associated with atopy (eczema, hay fever, allergy), occasionally with clear precipitants (e.g. allergens, cold air, smoking). In the clinic, emphasis will be on optimizing disease control, utilizing a stepwise escalation in medication beginning with short-acting beta agonists (SABAs, e.g. salbutamol) and inhaled steroids (e.g. beclometasone) to long-acting beta agonists (LABAs, e.g. salmeterol) and oral steroids. Aminophylline and anticholinergics (e.g. ipratropium) may also be added (see British Thoracic Society (BTS) guidelines: 
www.brit-thoracic.org.uk).
Is intermittent pharyngeal collapse in the obese. There is a characteristic history of snoring (and apnoeic episodes described by patients’ partners) and daytime somnolence. Treatment includes weight loss, CPAP, and surgery as a last resort.
Is a spectrum of lung disease due to smoking which encompasses chronic bronchitis (defined clinically) and emphysema (defined histologically). Elements of both are likely to be present. There is little or no reversibility of airway obstruction, minimal diurnal variation, and greater association with sputum production, chronic dyspnoea, and older age of onset (>35 years). Clinical presentation consists of persistent cough/sputum on most days for 3 months for 2 consecutive years. Manifestations of COPD as type 1 and type 2 respiratory failure are described as ‘pink puffer’ (normal/low PCO2 due to ventilation) and ‘blue bloater’ (cyanosis, hypercapnia with hypoxia driving ventilation) respectively. You will see these patients being managed in the ED following acute exacerbations, often infective, or end-stage in decompensated respiratory failure/cor pulmonale. Medical management is similar to asthma using bronchodilators and inhaled steroids, and stratified by severity as per BTS guidelines, with long-term oxygen therapy considered in later disease for some patients. (See Fig. 30.2.)
Fig. 30.2 Flow volume. Reproduced with permission from Jonathan Wilkinson et al, Thoracic Anaesthesia, 2011, Oxford University Press.
A multiorgan (pulmonary, neurological, cardiac, GI, cutaneous, etc.) syndrome of unknown cause resulting in granulomas. Pulmonary symptoms include dry cough, reduced exercise tolerance, and progressive dyspnoea. CXR may show bilateral hilar lymphadenopathy ± infiltrations, bullae, cysts, and fibrosis). Patients may also present with symptoms related to hypercalcaemia. Blood test shows elevated calcium and angiotensin-converting enzyme concentrations. Treat with immunosuppression (steroids, antimetabolites, biological, and chemotherapy, etc.).
Involves a mutation of the CFTR gene on chromosome 7 (incidence 1:2000, autosomal recessive). The pathology involves thick alveolar secretions chronic infection bronchiectasis. Complex cases may be managed in tertiary centres, receiving multidisciplinary respiratory support (antibiotics, mucolytics, bronchodilators), GI support (pancreatic enzyme replacement and nutritional supplementation), and fertility support, and may eventually require lung or liver transplant. Look for extrarespiratory signs.
Is a general term describing diffuse inflammation and/or fibrosis of the lung interstitium (i.e. space between alveoli). This restrictive pathology is most commonly idiopathic or can be associated with connective tissue disorders (SLE, RA), environmental exposure (asbestosis, bird droppings), and drugs (nitrofurantoin), etc. Regardless, the principles of treatment are similar: trigger avoidance, supplemental O2, and a trial of corticosteroids.
Is classified histologically into small cell (20%) or non-small cell (80% squamous, adenocarcinoma, large cell), and is primarily due to smoking. Presentation results from tumour mass (cough, wheeze, dyspnoea), local invasion (chest pain, haemoptysis, hoarse voice), and metastatic (bone pain) and paraneoplastic features (e.g. Cushing’s, hypercalcaemia). Attend the radiology MDT to observe imaging (CT, PET/CT, bone scan) and biopsy list in theatres (lung/lymph node where possible—bronchoscopic or transthoracic). These results assist with assessment and planning treatment. In general, most lung cancers have poor prognosis with small cell lung cancer generally disseminated at presentation, and relapse after chemotherapy with 3-month median survival (cf. 8 months for stage IV non-small cell lung cancer). Rarer cancers include malignant mesothelioma (related to asbestosis).
Is also a chronic obstructive airways disease, characterized by permanent dilatation of the bronchi due to destructive/inflammation from infection. Less common congenital causes include cystic fibrosis and those with primary immunodeficiencies. You can expect to see treatment with similar medications as COPD/asthma, with antibiotics for exacerbations. (See Fig. 30.3.)
Fig. 30.3 CXR showing abnormal dilatation of the airways of the right upper lobe. Appearances are that of bronchiectasis. The fine background reticular lung pattern may indicate interstitial lung disease. Reproduced with permission from Wilkinson, Ian, et al, Oxford Handbook of Clinical Medicine 10e, 2017: Oxford University Press. Image courtesy of Nottingham University Hospitals NHS Trust Radiology Department.
Plain radiographs of the chest provide important information and is a low-risk non-invasive investigation. The radiation dose is equivalent to 3 days’ worth of background radiation. Views include posteroanterior (PA) which is the most common, followed by anteroposterior (AP) which is usually done if the patient is too ill and supine, and lateral which is uncommon but helpful in delineating size and location of loculations for drainage under image guidance. These can be presented using the ABCDE method (see Fig. 30.4.)
Fig. 30.4 Chest radiograph. Amended from Wikipedia under creative commons license.
Endoscopy of the bronchial tree for diagnostics (malignancy, interstitial lung disease), and therapeutic purposes (aspiration mucus plugs). Most commonly flexible, but rigid under GA for retrieving a large foreign body and electrocautery for massive haemoptysis. The lung may be biopsied under image guidance (e.g. CT) transbronchially, percutaneously, or at video-assisted thoracic surgery (see 
pp. 643–644). Complications: infection, bleeding and perforation.
A tube into the pleural space to remove air/fluid/pus. You may see large-bore ‘surgical’ drains (e.g. trauma or draining haemothorax), while the respiratory ward is more likely to site Seldinger chest drains. Chest drain swinging—fluid in tube moving back and forth subtly with respiration—meaning the drain is in communication with the pleural space. Analysis of the fluid obtained—transudate vs exudate (including empyema) and Light’s criteria (pathology).
It is useful to have practised this first. Refer to a copy of predictive values to get an appreciation of numbers. This measures FEV1 values which are compared on a graph adjusted for age, height, and sex. Peak flow is often used to establish a rudimentary baseline of respiratory function and to observe effect of inhalers and nebulizers. Please find a suitable patient on the ward who is willing to perform one for you.
This is not a common investigation. However, if you have spare time during your block you may wish to find out if any are being conducted at your nuclear medicine department.
There will be a respiratory investigations department where spirometry takes place, typically for new diagnoses of lung disease and preoperative assessments. Familiarize yourself with the typical appearance of obstructive and restrictive flow loops. The most important values are FEV1—speed of flow (impaired in obstructive), FVC (reduced in restrictive disease); the FEV1/FVC ratio is in restrictive disease (reduction in FVC >>FEV1) and vice versa with obstructive disease.
Most students qualify without being able to confidently perform arterial blood for analysis. This will cause you many wasted hours stressed on-call without fulfilling a basic requirement of a junior doctor. Use this rotation to ensure you do not find yourself in this position as many respiratory patients require multiple arterial samples. Try to see arterial punctures in multiple locations (radial >femoral). Before arterial sampling of the wrist, perform Allen’s test.
You will never be required to state definitively whether a CTPA shows evidence or not of a PE; albeit, you might be interested and ask your consultant to point out key features of the CT (origin and path of the pulmonary artery) as it is relatively simple to see deficits representing embolus to impress your bosses in future.
Comes in two basic forms: CPAP continuous pressure support for type 1 respiratory failure represents splinting airway open (e.g. pulmonary oedema), and BPAP (bilevel positive airway pressure or non-invasive positive pressure ventilation) with IPAP pressure applied during triggered breaths and expiratory positive airway pressure (EPAP) (continuous positive pressure) between breaths.
• Airway: assess and manage airway using manoeuvres/adjuncts.
• Breathing: assess respiratory effort, 15 L/min O2, if no respiratory effort arrest team.
• Circulation: capillary refill time, pulse, BP, if no pulse arrest team.
Respiratory failure is failure of ventilation or gas exchange. Hypoxia can be due to V/Q mismatch (commonest), hypoventilation (+raised CO2), abnormal diffusion, right–left cardiac shunt. VQ mismatch may be due to inadequate ventilation (e.g. pneumonia) or inadequate perfusion (e.g. PE).
• Type I failure: PaO2 <8 kPa, PaCO2 <6 kPa
• Type II failure PaO2 <6 kPa, PaCO2 >6 kPa.
Implies infection within the airways. As a junior doctor, it is one of the pathologies that you will frequently encounter in ED/wards and should be familiar with assessment and management. Community-acquired pneumonia is commonly caused by Staphylococcus aureus and Streptococcus pneumoniae; hospital-acquired pneumonia is commonly caused by Gram-negative organisms; while aspiration pneumonia is commonly secondary to anaerobes. It is worth practising using the CURB-65 score as a guide to determine which patients should be admitted for treatment, and looking at the CXR of these patients (comparing them to previous CXRs). Also take blood samples, blood cultures, ABG (if hypoxic), sputum sample, and urinary antigens (pneumococcal and Legionella). Treatment is with oxygen (keep sats >94%), antibiotics, and hydration as well as steroid in asthma/COPD as per local protocol. Admit if CURB-65 score >2, hypoxic, septic, comorbidities, requiring IV antibiotics, or unable to cope at home. A repeat CXR is indicated 6 weeks afterwards which is the time it takes for radiological resolution to occur. (See Fig. 30.5.)
Fig. 30.5 Air space heterogeneous shadowing in the left upper zone with air bronchograms demonstrating a consolidation likely to represent pneumonia. However, since this is non-specific, you ought to rule out other differentials from a history and clinical examination. Reproduced with permission from Wilkinson, Ian, et al, Oxford Handbook of Clinical Medicine 10e, 2017: Oxford University Press. Image courtesy of Nottingham University Hospitals NHS Trust Radiology Department.
Is a simple, validated scoring system. See Table 30.1 and Table 30.2.
Table 30.1 CURB-65 scoring
| C | Confusion—abbreviated mental test ≤8/10 | 1 |
| U | Urea >7 mmol/L | 1 |
| R | Respiratory rate ≥30/min | 1 |
| B | BP <90 mmHg systolic and/or 60 mmHg diastolic | 1 |
| 65 | Age ≥65 years | 1 |
Table 30.2 CURB-65 scoring results
| Score | Mortality risk 30 days | Management |
| 0–1 | Mild (<3%) | Home treatment possible |
| 2 | Moderate (9%) | Hospital therapy |
| ≥3 | Severe (15–45%) | Severe pneumonia—consider ITU support |
Is characterized by the inability of complete full sentences, tachypnoea, PEFR <50%, with normal PaCO2. Beware of silent chest! You must elicit whether the patient has ever been intubated or admitted to ITU before. Also, look to exclude any triggering allergens and foreign travel. Triggers can be remembered as SAUCES:
Radiological signs include hyperinflation and diaphragm flattening but other pathologies such as pneumothorax, pneumomediastinum, and pneumonia ought to be excluded swiftly. (See Fig. 30.6.)
Fig. 30.6 Acute exacerbation of asthma. Reproduced with permission from Scott Moses, MD, www.fpnotebook.com.
The BTS has guidelines for each of these ( www.brit-thoracic.org.uk). Do not forget oxygen is a drug and should be prescribed, including flow rate, target SpO2, and mode of delivery (e.g. nasal prongs/face mask). Decide if the exacerbation is mild, moderate, severe, life-threatening, or near fatal (see Table 30.3).
Table 30.3 Asthma
| Moderate | Severe | Life-threatening | Near fatal |
| Increasing symptoms PEFR >50–75% best or predicted No features of acute severe asthma | Any 1 of: PEFR 33–50% best or predicted Resp. rate ≥25/min HR ≥110/min Inability to complete a sentence in one breath | Any 1 of: PEFR <33% best or predicted SpO2 <92% PaO2 <8 kPa Normal PaCO2 (4.6–6.0 kPa) Silent chest Cyanosis Poor respiratory effort Arrhythmia | PaCO2 and/or requiring mechanical ventilation with inflation pressures |
Be on the lookout for exhaustion as time goes by whereby the patient struggles to breathe more and more. Since younger patients have a greater physiological reserve whereby they can compensate for longer compared to the elderly, they can also deteriorate much more rapidly once decompensation occurs. If you struggle, it is best to call the on-call or crash team anaesthetist sooner rather than later. NIV followed by intubation may be the last resort but still takes time to prepare and set up before it could become too late.
Treatment can sometimes be very difficult as it may not always work. This is when you think of OH SPIT MAN (Table 30.4).
Table 30.4 OH SPIT MAN
| O | Oxygen (aim for SpO2 94–98%) |
| H | Hydration (IV fluids) |
| S | Salbutamol nebulizers (5 mg back-to-back if necessary) |
| P | Prednisolone (30–40 mg PO) or hydrocortisone (200 mg IV) |
| I | Ipratropium bromide (Atrovent®) nebulizers (5 mcg 4–6-hourly) |
| T | Transfer to HDU/ITU (if suspecting life-threatening asthma) |
| M | Magnesium sulfate |
| A | Aminophylline (antibiotics if infective cause) |
| N | NIV and intubation if tiring |
A classic exam scenario is the management of an asthmatic patient who deteriorates due to the development of a pneumothorax. Consider discharging patients whose PEFR is >75% best or predicted 1 hour after initial treatment. Give a 5-day course of prednisolone (30–40 mg once daily), check inhaler technique, and advise GP follow-up within the next 48 hours or to return to hospital if symptoms recur.
Consider the diagnosis in smokers >35 years with exertional breathlessness, chronic cough, regular sputum production, frequent winter 'bronchitis', or wheeze. Spirometry can support the diagnosis (FEV1/FVC ratio <0.7). An exacerbation is a sustained worsening of symptoms which is beyond normal day-to-day variations, and is acute in onset. Symptoms include worsening breathlessness, cough, sputum production, and change in sputum colour. Patients with COPD are at higher risk of acute deterioration, which is most commonly secondary to infection. Patients with asthma/COPD may benefit from specific antibiotics to cover certain organisms, as well as optimization of their chronic disease. Treatment is similar to asthma exacerbation with a few exceptions:
• Target SpO2 88–92% initially. If PaCO2 is normal adjust target to 94–98% (unless there is a history of NIV/intermittent positive pressure ventilation) and recheck ABGs after 30–60 min
• Nebulizers: salbutamol and ipratropium. If a patient is hypercapnic or acidotic the nebulizer should be driven by compressed air, not oxygen (to avoid worsening hypercapnia). Oxygen can be given simultaneously by nasal cannulae if needed.
• Prednisolone 30 mg PO for 7–14 days. Consider osteoporosis prophylaxis in patients requiring frequent courses of oral corticosteroids.
• NIV for persistent hypercapnic ventilatory failure despite optimal medical therapy. Before starting NIV, the ceiling of therapy should be agreed (i.e. is invasive ventilation appropriate?).
To ask the boss
• Consider the anti-inflammatory effect on chronic lung disease.
• Doubling steroid supplementation in steroid-dependent septic patient at risk of Addisonian crisis.
Describes an embolus thrombus in the pulmonary vasculature impairing gas exchange. Sudden-onset dyspnoea and pleuritic chest pain in the presence of type 1 respiratory failure. Other signs include syncope, haemoptysis, and even cardiac arrest in large PEs. Virchow’s triad describes risk factors for all VTEs including PEs. Practise calculating two-level Well’s scores1 to aid your diagnosis; <4 is unlikely and D-dimer may be used to rule out PE (sensitive not specific). (See Table 30.5.)
Table 30.5 Two-level PE Wells score
| Clinical feature | Points |
| Clinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins) | 3 |
| An alternative diagnosis less likely than PE | 3 |
| HR >100 bpm | 1.5 |
| Immobilization for >3 days or surgery in the previous 4 weeks | 1.5 |
| Previous DVT/PE | 1.5 |
| Haemoptysis | 1 |
| Malignancy (on treatment/treated in the last 6 months/palliative) | 1 |
| Clinical probability simplified scores | |
| PE likely | >4 |
| PE unlikely | <4 |
• ABG: may initially present with respiratory alkalosis from hyperventilating before decompensating (towards metabolic acidosis).
• ECG: may be normal or show sinus tachycardia, p pulmonale, AF, right bundle branch block, right axis deviation (‘S1’), Q wave and inverted T in III (‘Q3, T3’), T inversion in V1–4. S1Q3T3 on ECG is said to be pathognomonic but it is rare, and you are more likely to see a sinus tachycardia, right axis deviation, or right bundle branch block indicating right heart strain.
• CXR: to exclude other causes.
• FBC, INR, APTT, U&E: WCC may be high.
• CTPA: the gold standard; V/Q mismatch scan may be considered in pregnancy to avoid contrast and radiation.
• PE likely: immediate CTPA or if not available, parenteral anticoagulation followed by CTPA. Consider a proximal leg vein US scan if the CTPA is negative and DVT is suspected.
• PE unlikely: D-dimer, and if positive CTPA.
Usually consists of treatment dose of anticoagulation (LMWH/fondaparinux) within 24 hours for 5 days until warfarinized and INR ≥2; rarely haemodynamic instability necessitates unfractionated heparin and thrombolysis (know the contraindications). Warfarin needs to be continued for at least 3 months for first time VTE, extended therapy duration for second recurrence (if risk of bleeding is low), and indefinitely if recurrent VTEs with irreversible risk factors (deficiency in antithrombin III, protein S and C, factor V Leiden mutation, or the presence of antiphospholipid antibodies). If warfarin is unsuitable then consider rivaroxaban (factor Xa inhibitors). Thrombolectomy and vena cava filters are reserved as a last resort (especially if anticoagulation is contraindicated or recurrent PEs occur despite INR target of 3–4).
Causes for PE/VTE consist of I STOP OCPs (or I POST COPS):
| I | Immobility |
| S | Surgery |
| T | Thrombophilia |
| O | Obesity |
| P | Pregnancy |
| O | Oral contraceptive pill (OCP) |
| C | Cancer |
| P | Previous VTE |
| S | Smoking. |
Is fluid (blood (haemothorax), lymph fluid (chylothorax), pus (empyema)) within the pleural space. You will be expected to know about ten different causes for your finals but to sound slick remember to always ‘classify or die’ (Table 30.6). The effusion is either a transudate (mainly intrinsic organ failure from increasing hydrostatic and reduced osmotic pressures) or exudate depending on the protein content. Light’s criteria will determine samples in between 25-30 g/dl of protein content.
Table 30.6 Pleural effusion
Is air leaking into the pleural space. Spontaneous (primary) in young, tall, thin males, secondary to asthma/COPD (from bullae) and traumatic from penetrating injury (e.g. subclavian lines). Presentation is variable, and treatment depends on symptoms and size of pneumothorax with decompression pleurocentesis followed by chest drains. It is important for you to identify the admitted patients on the ward with treated pneumothoraces to appreciate the pre- and post-decompression plain films. (See Fig. 30.7.)
Fig. 30.7 Left tension pneumothorax. Note delineated area with absent lung markings, the tracheal deviation, and movement of the heart away from the affected side. Amended from Wikimedia under creative commons licence.
Management is determined by the size as measured at the level of the hila (large >2 cm, small <2 cm) and whether there is dyspnoea (see Fig. 30.8 for BTS guidelines).
Fig. 30.8 BTS guidelines on managing spontaneous pneumothorax. Reproduced with permission from MacDuff, Andrew, et al, Management of spontaneous pneumothorax: British Thoracic Society pleural disease guideline 2010, Thorax, 2010, Vol 65 Supp. II.
Is fluid accumulation in the interstitium and air spaces. It is often cardiogenic and always resulting from damage to the vasculature and/or lung parenchyma. Management is ensuring adequate oxygenation (e.g. supplemental oxygen and positive pressure) and other treatments include glyceryl trinitrate (to reduce venous return) and loop diuretics (to offload fluid). (See Fig. 30.9.)
Fig. 30.9 Widespread reticulonodular shadowing showing both interstitial and alveolar pulmonary oedema. Classic signs include ABCDE. Amended from Wiki-media under creative commons Attribution-Share Alike 3.0 Un-ported license.
Honours
Leads to hypoxia which can be explained by the dissociation curves for O2 and CO2: OxyHb is already saturated at >90% and therefore there is little ‘space’ for compensation by functional lung units. In comparison, greater amounts of CO2 can be exchanged from the blood into functional lung units, normal CO2 levels.
D-dimer is a breakdown product of a thrombus (e.g. DVT) but may be raised (e.g. false positives) in the LIMPS:
• Infection and Inflammation (including autoimmune)
Causes include sarcoidosis, lymphoma, and TB.
There was a time when every baby was inoculated with BCG after birth. Then came a time where only high-risk populations were vaccinated (e.g. Indian sub-continent and African origins). With an increasing migrant population, there has been a resurgence of TB. The Mycobacterium tuberculosis infection may be latent and present with systemic symptoms. Pulmonary symptoms include cough/sputum, pleurisy, haemoptysis, pleural effusion with constitutional symptoms including anorexia, weight loss, malaise, and night sweats. CXRs may show consolidations, fibrosis, and calcifications which may represent the hallmark pathology of caseating granulomas known as Gohn’s focus/complex. Miliary TB results from haematogenous spread and shows up as widespread millets on both lung fields. At least three sputum samples need to be sent to the lab to test for acid–fast bacilli (AFB), and culture and sensitivity. Other immunological tests consist of tuberculin skin test, QuantiFERON TB Gold® and T-SPOT®.TB tests which have replaced the older Mantoux testing. While waiting for the lab results, quadruple drug therapy is instigated in two phases.
See Table 30.7 and Table 30.8.
Table 30.7 Pulmonary tuberculosis: side effects of drugs
| Drug | Side effects |
| Rifampicin | Hepatitis, orange-staining of tears and urine |
| Isoniazid | Hepatitis, neuropathy, agranulocytosis |
| Pyrazinamide | Hepatitis, arthralgia |
| Ethambutol | Optic neuritis (colour vision first) |
Table 30.8 Recent studies in respiratory medicine
| Details | Trial | Comments |
| 2003 JAMA N = 314 | Reduction in the Use of Corticosteroids in Exacerbated COPD (REDUCE) | A 5-day course of glucocorticoids is non-inferior to a 14-day course for treating acute COPD exacerbations and preventing further exacerbations |
| 2003 JAMA N = 401 | PneumA (randomized, controlled trial) | Equivalent mortality in ventilator-associated pneumonia treated with 8 vs 15 days of antibiotic therapy, except for Pseudomonas aeruginosa |
| 2006 NEJM N = 824 | Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED | 83% sensitivity and 96% specificity with CT angiography in detecting acute PE including strongly correlating with pre-test probability with Well’s score |
| 2011 NEJM | National Lung Cancer Screening (NLST) | Low-dose screening CT scans reduce lung cancer mortality compared to CXR |
All four drugs are given for 8 weeks and then only rifampicin and isoniazid are continued for another 16 weeks. Pyridoxine (vitamin B6) should be supplemented to counteract isoniazid toxicity.
Reference
1. Wells PS, Anderson DR, Rodger M, et al. (2000). Derivation of a simple clinical model to categorise patients' probability of pulmonary embolism: increasing the model's utility with the SimpliRED D-dimer. Thromb Haemost 83:416–20.
Most respiratory patients are stable and chronically unwell and in abundant supply for medical school examinations.
Common symptoms reported will be progressive shortness of breath, coughing up sputum/blood, and chest tightness. Again, a focused history is key for you not to waste time chasing red herrings. Also remember that respiratory symptoms may also originate from cardiogenic (e.g. cardiogenic asthma) and GI (e.g. dyspepsia, GORD) causes. Make sure you ask about previous need for intubation or ITU admission for asthmatic/COPD patients to give you an idea of how severe their disease is. Key elements to check include travel history, pet exposure, occupation, smoking, and allergies/atopy.
In all respiratory examinations expect paraphernalia around the bed—inhalers, oxygen cylinders, etc. There are more things to see at the end of the bed looking at a respiratory patient than most other patients. Practise this on every ward round.
This requires you to do your examination thoroughly. A good inspection for previous scars especially around the back is crucial. Remember sensible suggestions in finals (i.e. tension pneumothorax less than likely).
Practise your percussion on the respiratory ward; you should practise ‘feeling’ the difference between stony dull effusion, dull consolidation, resonant normality, and hyper-resonance in asthma and pneumothorax. Ask your partner to stand at the other side of the bay and also listen to the percussion note. The quality of medical students can sometimes be judged by bizarre indicators and a strong percussion note is indicative of this.
For instance, look for the barrel-chested obese patient with inhalers by the bedside, be open to hyperexpansion on palpation and hyper-resonance on percussion.
Always mention to patients what you are going to be doing next and warn them when they may feel discomfort (e.g. feeling for the trachea).