The management of asthma in adults has been updated by NICE in 2017, following the 2016 BTS guidelines. One of the significant changes is in ‘step 3’, where patients on a SABA + ICS whose asthma is not well controlled should be offered a leukotriene receptor antagonist instead of a LABA. NICE does not follow the stepwise approach of the previous BTS guidelines, but to make the guidelines easier to follow, we have added our own steps. The steps range from newly-diagnosed asthma to SABA +/- LTRA + one of the following options, including increasing ICS to high-dose, a trial of an additional drug, or seeking advice from a healthcare professional with expertise in asthma. Maintenance and reliever therapy (MART) is a form of combined ICS and LABA treatment that is only available for ICS and LABA combinations in which the LABA has a fast-acting component. It should be noted that NICE does not recommend changing treatment in patients who have well-controlled asthma simply to adhere to the latest guidance. The definitions of what constitutes a low, moderate, or high-dose ICS have also changed, with <= 400 micrograms budesonide or equivalent being a low dose, 400 micrograms - 800 micrograms budesonide or equivalent being a moderate dose, and > 800 micrograms budesonide or equivalent being a high dose for adults.

An anion gap greater than 14 mmol/L typically indicates a raised anion gap metabolic acidosis, rather than a normal anion gap. In the absence of other information about the patient, an arterial blood gas (ABG) can provide a clue to the diagnosis. In this case, the ABG shows a normal paO2, indicating a respiratory cause of the patient’s symptoms is less likely. However, the pH is below 7.35, indicating acidosis, and the bicarbonate is low, suggesting metabolic acidosis. The low paCO2 shows partial compensation. Calculating the anion gap reveals a value of 31 mmol/L, indicating metabolic acidosis with a raised anion gap. Septic shock is the only listed cause of raised anion gap metabolic acidosis, resulting in acidosis due to the production of lactic acid from inadequate tissue perfusion. Addison’s disease is another cause of metabolic acidosis, but it results in normal anion gap metabolic acidosis due to bicarbonate loss from mineralocorticoid deficiency. Prolonged diarrhea can cause normal anion gap metabolic acidosis due to gastrointestinal loss of bicarbonate. Pulmonary embolism is unlikely due to normal oxygen levels and hypocapnia occurring as compensation. Prolonged vomiting can cause metabolic alkalosis, not metabolic acidosis, due to the loss of hydrogen ions in vomit. This patient’s electrolyte profile does not fit with prolonged vomiting.

The anion gap is a measure of the difference between positively charged ions (sodium and potassium) and negatively charged ions (bicarbonate and chloride) in the blood. It is calculated by subtracting the sum of bicarbonate and chloride from the sum of sodium and potassium. A normal anion gap falls between 8-14 mmol/L. This measurement is particularly useful in diagnosing metabolic acidosis in patients.

There are various causes of a normal anion gap or hyperchloraemic metabolic acidosis. These include gastrointestinal bicarbonate loss due to conditions such as diarrhoea, ureterosigmoidostomy, or fistula. Renal tubular acidosis, drugs like acetazolamide, ammonium chloride injection, and Addison’s disease can also lead to a normal anion gap.

On the other hand, a raised anion gap metabolic acidosis can be caused by lactate due to shock or hypoxia, ketones in conditions like diabetic ketoacidosis or alcoholism, urate in renal failure, acid poisoning from substances like salicylates or methanol, and 5-oxoproline from chronic paracetamol use. Understanding the anion gap and its potential causes can aid in the diagnosis and treatment of metabolic acidosis.

Paraneoplastic syndromes are a group of disorders that can occur in patients with certain types of cancer, but are not caused by metastases, infections, metabolic disorders, chemotherapy, or coagulation disorders. These syndromes can present with a variety of symptoms affecting different body systems. Some of these syndromes are specific to certain types of cancer and may be the first sign of the disease. Therefore, if a patient presents with symptoms of a paraneoplastic syndrome, it is important to consider the possibility of an underlying malignancy. While certain paraneoplastic syndromes are associated with specific types of cancer, there can be some overlap.

Prior infection with influenza increases the likelihood of developing pneumonia caused by Staphylococcus aureus.

Causes of Pneumonia

Pneumonia is a respiratory infection that can be caused by various infectious agents. Community acquired pneumonia (CAP) is the most common type of pneumonia and is caused by different microorganisms. The most common cause of CAP is Streptococcus pneumoniae, which accounts for around 80% of cases. Other infectious agents that can cause CAP include Haemophilus influenzae, Staphylococcus aureus, atypical pneumonias caused by Mycoplasma pneumoniae, and viruses.

Klebsiella pneumoniae is another microorganism that can cause pneumonia, but it is typically found in alcoholics. Streptococcus pneumoniae, also known as pneumococcus, is the most common cause of community-acquired pneumonia. It is characterized by a rapid onset, high fever, pleuritic chest pain, and herpes labialis (cold sores).

In summary, pneumonia can be caused by various infectious agents, with Streptococcus pneumoniae being the most common cause of community-acquired pneumonia. It is important to identify the causative agent to provide appropriate treatment and prevent complications.

Spirometry: The Best Diagnostic Tool for COPD

Chronic obstructive pulmonary disease (COPD) is a common respiratory condition that can significantly impact a patient’s quality of life. To diagnose COPD, spirometry is the best diagnostic tool. According to NICE guidelines, a diagnosis of COPD should be made based on symptoms and signs, but supported by spirometry results. Post-bronchodilator spirometry should be performed to confirm the diagnosis. Airflow obstruction is confirmed by a forced expiratory volume in 1 s (FEV1):forced vital capacity (FVC) ratio of <0.7 and FEV1 <80% predicted. Other diagnostic tools, such as CT of the chest, serial peak flow readings, and trials of beclomethasone or salbutamol, may have a role in the management of COPD, but they are not used in the diagnosis of the condition. CT of the chest may be used to investigate symptoms that seem disproportionate to the spirometric impairment, to investigate abnormalities seen on a chest radiograph, or to assess suitability for surgery. Serial peak flow readings may be appropriate if there is some doubt about the diagnosis, in order to exclude asthma. Inhaled corticosteroids and short-acting beta agonists may be used in the management of COPD for breathlessness/exercise limitation, but they are not used in the diagnosis of COPD. In summary, spirometry is the best diagnostic tool for COPD, and other diagnostic tools may have a role in the management of the condition.

Understanding Bronchiectasis: Causes, Symptoms, and Treatment

Bronchiectasis is a condition characterized by permanent and irreversible dilatations of the bronchial walls. It can be caused by various factors, including cystic fibrosis, immune system deficiencies, lung infections, foreign body aspiration, and smoking. Common symptoms of bronchiectasis include high sputum production, recurrent chest infections, and haemoptysis. A high-resolution computed tomography (HR-CT) scan of the lungs is usually used to diagnose bronchiectasis. Treatment involves a multidisciplinary approach, including chest physiotherapy, patient education, antibiotic treatment, and bronchodilators. While treatment of the underlying cause may be necessary, it does not provide reversal of the existing bronchiectasis. Other conditions, such as atypical pneumonia, lung cancer, tuberculosis, and pulmonary embolism, may have similar symptoms but require different diagnoses and treatments.

Understanding the CURB-65 Score for Mortality Prediction in Pneumonia

Pneumonia is a serious respiratory infection that can lead to mortality, especially in older patients. Several factors can increase the risk of death, including elevated urea levels, low blood pressure, leukopenia, and atrial fibrillation. To predict mortality in pneumonia, healthcare professionals use the CURB-65 score, which considers five parameters: confusion, urea >7 mmol/l, respiratory rate >30/min, systolic blood pressure <90 mmHg or diastolic blood pressure <60 mmHg, and age >65 years. Each parameter scores a point, and the higher the total score, the higher the associated mortality.

Based on the CURB-65 score, healthcare professionals can make informed decisions about treatment and admission to hospital. Patients with a score of 0 or 1 can be treated at home with oral antibiotics, while those with a score of 2 should be considered for hospital admission. Patients with a score of 3 or higher should be admitted to hospital, and those with a score of 4-5 may require high dependency or intensive therapy unit admission. However, individual circumstances, such as the patient’s performance status, co-morbidities, and social situation, should also be considered when making treatment decisions.

In summary, the CURB-65 score is a valuable tool for predicting mortality in pneumonia and guiding treatment decisions. By considering multiple factors, healthcare professionals can provide the best possible care for patients with this serious infection.

Exacerbations of chronic obstructive pulmonary disease (COPD) are a common occurrence and can be caused by various factors, including bacterial infections. In a bacterial acute exacerbation of chronic obstructive pulmonary disease, the most common causative pathogens are Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. Since the introduction of the pneumococcal conjugate vaccine, the most common bacterial pathogen may be changing from Streptococcus pneumoniae to Haemophilus influenzae and Moraxella catarrhalis. Mycoplasma pneumoniae and Chlamydia pneumoniae are also relatively common. An elevated white cell count may indicate exacerbation, but a lack of prominent leukocytosis is common. Clinical judgement is crucial, and a C-reactive protein (CRP) test may be useful, but it lags behind by 24-48 hours.

Exacerbations of COPD are characterized by episodes of acutely increased dyspnea and cough, often with a change in the characteristics of the sputum. Despite fever and other signs and symptoms, the clinical presentation is mild to moderate in most cases. Patients with COPD often develop type 2 respiratory failure, which can escalate into respiratory acidosis, a potentially serious complication that may require non-invasive or invasive ventilation. An arterial blood gas analysis should be performed early in every patient presenting with a possible exacerbation of COPD.

Treatment options for bacterial infections in exacerbations of COPD include trimethoprim-sulfamethoxazole (Septrin) combinations. However, resistance to this combination has been frequently reported in cases of infection with M. catarrhalis. The vast majority of cases of infection with M. catarrhalis are also penicillin-resistant due to their production of beta-lactamase. Co-amoxiclav is usually the antibiotic of choice, with macrolides being good alternatives.  In most cases, the initial antibiotic treatment is empirical and mainly guided by known local sensitivities and the patient’s previous history of exacerbations. Gram stain can be quite useful to identify broad classes of bacteria. If the gram stain is inconclusive, blood cultures should be performed if the patient is pyrexial.

Assessing the Need for Oxygen Therapy in Patients with Respiratory Conditions

When assessing the need for oxygen therapy in patients with respiratory conditions, it is important to consider various factors. For instance, NICE recommends LTOT for patients with a PaO2 between 7.3 and 8.0 kPa when stable, if they have comorbidities such as secondary polycythaemia, peripheral oedema, or pulmonary hypertension. Additionally, patients with very severe or severe airflow obstruction, cyanosis, raised jugular venous pressure, and oxygen saturations ≤92% when breathing air should also be assessed for oxygen therapy.

However, it is important to note that a non-smoker with a PaO2 of 8.2 kPa with pulmonary hypertension does not meet the criteria for oxygen therapy, while a non-smoker with FEV1 56% or a non-smoker with a PaO2 of 7.6 kPa and diabetes mellitus also do not meet the criteria for LTOT. On the other hand, a smoker with a PaO2 of 7.3 kPa may be considered for oxygen therapy, but it is important to ensure that the result has been checked twice and to warn the patient about the risks of smoking while on oxygen therapy.

The treatment of tuberculosis is a complex process that requires the expertise of a specialist in the field, such as a respiratory physician or an infectivologist. The first-line drugs used for active tuberculosis without CNS involvement are isoniazid, rifampicin, pyrazinamide, and ethambutol. These drugs are given together for the first 2 months of therapy, followed by continued treatment with just isoniazid and rifampicin for an additional 4 months. Pyridoxine is added to the treatment regimen to reduce the risk of isoniazid-induced peripheral neuropathy. If there is CNS involvement, the four drugs (and pyridoxine) are given together for 2 months, followed by continued treatment with isoniazid (with pyridoxine) and rifampicin for an additional 10 months. It is important to monitor liver function tests before and during treatment, and to educate patients on the potential side effects of the drugs and when to seek medical attention. Treatment-resistant tuberculosis cases are becoming more common and require special management and public health considerations.

Understanding Cryptogenic Fibrosing Alveolitis

Cryptogenic fibrosing alveolitis, also known as idiopathic pulmonary fibrosis, is a disorder that typically affects individuals between the ages of 50 and 70 years, with a slightly higher incidence in men than women. The condition is characterized by progressive breathlessness on exertion, dry cough, and a restrictive pattern on pulmonary function tests. While excessive sputum production is uncommon in the early stages, constitutional symptoms such as weight loss and lethargy may occur. Finger clubbing is a common finding in patients with cryptogenic fibrosing alveolitis.

While haemoptysis is rare, it may suggest the development of lung malignancy, which occurs with an increased risk in patients with this condition. It is important to note that the risk of lung cancer does not exclude the possibility of cryptogenic fibrosing alveolitis. Chest pain is uncommon in this condition.

There is no definitive treatment for cryptogenic fibrosing alveolitis, and the average survival from the time of diagnosis is 3 years. However, the course of the disease can be highly variable, and up to 20% of patients survive for more than 5 years from diagnosis.

In summary, cryptogenic fibrosing alveolitis is a progressive lung disorder that presents with breathlessness on exertion, dry cough, and a restrictive pattern on pulmonary function tests. While there is no definitive treatment, early diagnosis and management can improve outcomes for patients.

Amiodarone is known to cause pulmonary fibrosis, which is evident in the patient’s symptoms of dyspnea and restrictive lung disease on spirometry. However, other potential causes of restrictive lung disease should be investigated before attributing it solely to amiodarone use. Amiodarone can also lead to liver injury and thyroid dysfunction, so monitoring liver and thyroid function is important during treatment.

Ramipril, an ACE inhibitor, commonly causes a persistent dry cough, which is the most frequently reported side effect and often leads to discontinuation of treatment. The exact mechanism of cough production is unclear, but it may involve increased levels of kinins and substance P due to ACE inhibition. Substituting with another antihypertensive drug, such as an angiotensin II receptor blocker, is typically necessary to alleviate the cough.

Aspirin can exacerbate asthma in susceptible individuals, particularly those with Samter’s triad (nasal polyps, asthma, and aspirin sensitivity). However, the patient’s restrictive lung disease is not associated with aspirin use.

Beta blockers like bisoprolol can cause bronchoconstriction in patients with asthma and COPD, making them contraindicated in asthma and requiring caution in COPD. However, the patient’s spirometry results suggest pulmonary fibrosis rather than bronchospasm.

Furosemide can rarely cause bronchoconstriction, but it is not associated with the restrictive lung disease seen in this patient.

According to NICE 2017 guidelines, if a patient with asthma is not effectively managed with a SABA + ICS, the first step should be to add a LTRA rather than a LABA.

The management of asthma in adults has been updated by NICE in 2017, following the 2016 BTS guidelines. One of the significant changes is in ‘step 3’, where patients on a SABA + ICS whose asthma is not well controlled should be offered a leukotriene receptor antagonist instead of a LABA. NICE does not follow the stepwise approach of the previous BTS guidelines, but to make the guidelines easier to follow, we have added our own steps. The steps range from newly-diagnosed asthma to SABA +/- LTRA + one of the following options, including increasing ICS to high-dose, a trial of an additional drug, or seeking advice from a healthcare professional with expertise in asthma. Maintenance and reliever therapy (MART) is a form of combined ICS and LABA treatment that is only available for ICS and LABA combinations in which the LABA has a fast-acting component. It should be noted that NICE does not recommend changing treatment in patients who have well-controlled asthma simply to adhere to the latest guidance. The definitions of what constitutes a low, moderate, or high-dose ICS have also changed, with <= 400 micrograms budesonide or equivalent being a low dose, 400 micrograms - 800 micrograms budesonide or equivalent being a moderate dose, and > 800 micrograms budesonide or equivalent being a high dose for adults.

Understanding PEFR and Its Role in Diagnosing Asthma

Peak expiratory flow rate (PEFR) is a valuable tool in both the diagnosis and management of asthma. It is measured by a maximal forced expiration through a peak-flow meter and correlates well with forced expiratory volume in one second (FEV1), providing an estimate of airway calibre. Patients with asthma can monitor their PEFR at home to track disease control. A PEFR <80% of predicted is a strong indicator of obstructive airway disease, such as asthma. However, it’s important to note that PEFR is not affected by restrictive defects, such as those caused by kyphoscoliosis. Bronchial carcinoma itself does not cause airflow limitation, but a co-morbid obstructive lung disease, such as asthma or COPD, could produce abnormal PEFR readings. Bronchiectasis can cause an obstructive pattern on spirometry, but it would not typically cause a reduction in PEFR. Whooping cough, despite causing inflammation of the airways, would not typically result in the markedly reduced PEFR readings seen in asthma. In conclusion, understanding PEFR and its role in diagnosing asthma is crucial for both patients and healthcare providers. By monitoring PEFR at home and seeking medical attention when necessary, individuals with asthma can better manage their condition and improve their quality of life.

Diagnostic Tests for Alpha-1-Antitrypsin Deficiency

Alpha-1-antitrypsin deficiency (AATD) is a genetic disorder that can lead to chronic obstructive pulmonary disease (COPD) at a young age, especially in non-smokers with a family history of the condition. Here are some diagnostic tests that can help identify AATD:

Blood Test: A simple blood test can measure the levels of alpha-1-antitrypsin in the blood. Low levels of this protein can indicate AATD, especially in patients with symptoms of COPD or a family history of the condition.

CT Chest: A computed tomography (CT) scan of the chest can reveal the extent and pattern of emphysema in the lungs, which is a common complication of AATD. However, a CT scan alone cannot diagnose AATD.

Chest X-Ray: A chest X-ray (CXR) can also show signs of emphysema or bronchiectasis in patients with AATD, but it is not a definitive test for the condition.

Genetic Testing: Once AATD has been diagnosed, genetic testing can identify the specific variant of the condition that a patient has. However, genetic testing is not useful as an initial diagnostic test without first confirming low levels of alpha-1-antitrypsin in the blood.

Pulmonary Function Testing: This test measures lung function and can help assess the severity of lung disease in patients with AATD. However, it is not a diagnostic test for the condition.

In conclusion, a combination of these diagnostic tests can help identify AATD in patients with symptoms of COPD, a family history of the condition, or low levels of alpha-1-antitrypsin in the blood.

According to the British Thoracic Society (BTS), chest tube placement in pleural infection is mainly indicated for patients with purulent or cloudy pleural fluid, positive Gram stain and/or culture results from non-purulent pleural fluid, and pleural fluid pH below 7.2. Among these indications, pleural fluid pH is considered the most valuable test.

Investigating and Managing Pleural Effusion: BTS Guidelines

Pleural effusion is a condition where fluid accumulates in the pleural space, the area between the lungs and the chest wall. To investigate and manage this condition, the British Thoracic Society (BTS) has provided guidelines.

Imaging is an essential part of the investigation process, and the BTS recommends performing posterioranterior (PA) chest x-rays in all patients. Ultrasound is also recommended as it increases the likelihood of successful pleural aspiration and is sensitive for detecting pleural fluid septations. Contrast CT is increasingly performed to investigate the underlying cause, particularly for exudative effusions.

Pleural aspiration is another crucial step in the investigation process. The BTS recommends using ultrasound to reduce the complication rate. A 21G needle and 50ml syringe should be used, and fluid should be sent for pH, protein, lactate dehydrogenase (LDH), cytology, and microbiology. Light’s criteria can help distinguish between a transudate and an exudate. Other characteristic pleural fluid findings include low glucose in rheumatoid arthritis and tuberculosis, raised amylase in pancreatitis and oesophageal perforation, and heavy blood staining in mesothelioma, pulmonary embolism, and tuberculosis.

In cases of pleural infection, diagnostic pleural fluid sampling is required for all patients with a pleural effusion in association with sepsis or a pneumonic illness. If the fluid is purulent or turbid/cloudy, a chest tube should be placed to allow drainage. If the fluid is clear but the pH is less than 7.2 in patients with suspected pleural infection, a chest tube should be placed.

For managing recurrent pleural effusion, options include recurrent aspiration, pleurodesis, indwelling pleural catheter, and drug management to alleviate symptoms such as opioids to relieve dyspnoea. The BTS guidelines provide a comprehensive approach to investigating and managing pleural effusion.

Once the predicted values are obtained, the FEV1:FVC ratio can be evaluated. If this ratio is less than 70, it indicates a potential issue.

Understanding Idiopathic Pulmonary Fibrosis

Idiopathic pulmonary fibrosis (IPF) is a chronic lung condition that causes progressive fibrosis of the interstitium of the lungs. Unlike other causes of lung fibrosis, IPF has no underlying cause. It is typically seen in patients aged 50-70 years and is more common in men.

The symptoms of IPF include progressive exertional dyspnoea, dry cough, clubbing, and bibasal fine end-inspiratory crepitations on auscultation. Diagnosis is made through spirometry, impaired gas exchange tests, and imaging such as chest x-rays and high-resolution CT scans.

Management of IPF includes pulmonary rehabilitation, but very few medications have been shown to be effective. Some evidence suggests that pirfenidone, an antifibrotic agent, may be useful in selected patients. Many patients will eventually require supplementary oxygen and a lung transplant.

The prognosis for IPF is poor, with an average life expectancy of around 3-4 years. CT scans can show advanced pulmonary fibrosis, including honeycombing. While there is no cure for IPF, early diagnosis and management can help improve quality of life and potentially prolong survival.

Management of Acute Asthma

Acute asthma is classified by the British Thoracic Society (BTS) into three categories: moderate, severe, and life-threatening. Patients with any of the life-threatening features should be treated as having a life-threatening attack. A fourth category, Near-fatal asthma, is also recognized. Further assessment may include arterial blood gases for patients with oxygen saturation levels below 92%. A chest x-ray is not routinely recommended unless the patient has life-threatening asthma, suspected pneumothorax, or failure to respond to treatment.

Admission criteria include a previous near-fatal asthma attack, pregnancy, an attack occurring despite already using oral corticosteroid, and presentation at night. All patients with life-threatening asthma should be admitted to the hospital, and patients with features of severe acute asthma should also be admitted if they fail to respond to initial treatment. Oxygen therapy should be started for hypoxaemic patients. Bronchodilation with short-acting beta₂-agonists (SABA) is recommended, and all patients should be given 40-50mg of prednisolone orally daily. Ipratropium bromide and IV magnesium sulphate may also be considered for severe or life-threatening asthma. Patients who fail to respond require senior critical care support and should be treated in an appropriate ITU/HDU setting. Criteria for discharge include stability on discharge medication, checked and recorded inhaler technique, and PEF levels above 75% of best or predicted.

Guidelines for Emergency Oxygen Therapy

The British Thoracic Society has updated its guidelines for emergency oxygen therapy in 2017. The guidelines recommend that in critically ill patients, such as those experiencing anaphylaxis or shock, oxygen should be administered via a reservoir mask at 15 l/min. However, certain conditions, such as stable myocardial infarction, are excluded from this recommendation.

The guidelines also provide specific oxygen saturation targets for different patient groups. Acutely ill patients should aim for a saturation range of 94-98%, while patients at risk of hypercapnia, such as those with COPD, should aim for a lower range of 88-92%. Oxygen therapy should be reduced in stable patients with satisfactory oxygen saturation.

For COPD patients, a 28% Venturi mask at 4 l/min should be used prior to availability of blood gases. The target oxygen saturation range for these patients should be 88-92% if they have risk factors for hypercapnia but no prior history of respiratory acidosis. If the pCO2 is normal, the target range can be adjusted to 94-98%.

The guidelines also highlight situations where oxygen therapy should not be used routinely if there is no evidence of hypoxia. These include myocardial infarction and acute coronary syndromes, stroke, obstetric emergencies, and anxiety-related hyperventilation.

Overall, these guidelines provide clear recommendations for the administration of emergency oxygen therapy in different patient groups and situations.

According to NICE (2017) guidelines, patients with asthma should be prescribed a SABA as the first step of treatment. However, if a patient experiences symptoms three or more times per week or night waking, they should also be prescribed a low-dose ICS inhaler as the second step of treatment. This is also necessary for patients who have had an acute exacerbation requiring oral corticosteroids in the past two years. In this case, the patient’s symptoms are not well-controlled with a SABA alone, and she experiences frequent symptoms and night waking. Therefore, she requires a low-dose ICS inhaler, and the only option available is budesonide.

Adding a salmeterol inhaler is not appropriate at this stage, as LABAs are only used as the fourth step of treatment if a patient is not controlled with a SABA, low-dose ICS, and a trial of LTRAs. Similarly, adding montelukast and a beclomethasone inhaler is not appropriate, as LTRAs are only added if a patient is still not controlled on a low-dose ICS and a SABA. However, it may be appropriate to trial beclomethasone without montelukast.

Continuing with the current salbutamol-only treatment is not appropriate, as the patient’s asthma is poorly controlled, which increases the risk of morbidity and mortality. Regular salbutamol has no role in the management of asthma, as it does not improve outcomes and may even worsen them by downregulating beta receptors that are important for bronchodilation.

The management of asthma in adults has been updated by NICE in 2017, following the 2016 BTS guidelines. One of the significant changes is in ‘step 3’, where patients on a SABA + ICS whose asthma is not well controlled should be offered a leukotriene receptor antagonist instead of a LABA. NICE does not follow the stepwise approach of the previous BTS guidelines, but to make the guidelines easier to follow, we have added our own steps. The steps range from newly-diagnosed asthma to SABA +/- LTRA + one of the following options, including increasing ICS to high-dose, a trial of an additional drug, or seeking advice from a healthcare professional with expertise in asthma. Maintenance and reliever therapy (MART) is a form of combined ICS and LABA treatment that is only available for ICS and LABA combinations in which the LABA has a fast-acting component. It should be noted that NICE does not recommend changing treatment in patients who have well-controlled asthma simply to adhere to the latest guidance. The definitions of what constitutes a low, moderate, or high-dose ICS have also changed, with <= 400 micrograms budesonide or equivalent being a low dose, 400 micrograms - 800 micrograms budesonide or equivalent being a moderate dose, and > 800 micrograms budesonide or equivalent being a high dose for adults.

Risk Factors for Lung Cancer

Lung cancer is a deadly disease that can be caused by various factors. The most significant risk factor for lung cancer is smoking, which increases the risk by a factor of 10. However, other factors such as exposure to asbestos, arsenic, radon, nickel, chromate, and aromatic hydrocarbon can also increase the risk of developing lung cancer. Additionally, cryptogenic fibrosing alveolitis has been linked to an increased risk of lung cancer.

It is important to note that not all factors are related to lung cancer. For example, coal dust exposure has not been found to increase the risk of lung cancer. However, smoking and asbestos exposure are synergistic, meaning that a smoker who is also exposed to asbestos has a 50 times increased risk of developing lung cancer (10 x 5). Understanding these risk factors can help individuals make informed decisions about their health and take steps to reduce their risk of developing lung cancer.

The recommended treatment for acute pulmonary oedema in this patient is IV loop diuretic, specifically furosemide. This is because the patient is experiencing acute decompensated heart failure, which causes pulmonary oedema. IV loop diuretic has a prompt diuretic effect, reducing ventricular filling pressures and improving symptoms within 30 minutes.

IV dobutamine is not necessary for this patient as they are not in shock and dobutamine is typically reserved for patients with severe left ventricular dysfunction who have potentially reversible cardiogenic shock.

IV morphine is not recommended for acute heart failure as it may increase morbidity in patients with acute pulmonary oedema.

Oral furosemide is not the preferred route of administration for this patient as IV furosemide has a faster onset of diuresis.

Heart failure requires acute management, with recommended treatments for all patients including IV loop diuretics such as furosemide or bumetanide. Oxygen may also be necessary, with guidelines suggesting oxygen saturations be kept at 94-98%. Vasodilators such as nitrates should not be routinely given to all patients, but may have a role in cases of concomitant myocardial ischaemia, severe hypertension, or regurgitant aortic or mitral valve disease. However, hypotension is a major side-effect/contraindication. Patients with respiratory failure may require CPAP, while those with hypotension or cardiogenic shock may require inotropic agents like dobutamine or vasopressor agents like norepinephrine. Mechanical circulatory assistance such as intra-aortic balloon counterpulsation or ventricular assist devices may also be necessary. Regular medication for heart failure should be continued, with beta-blockers only stopped in certain circumstances. Opiates should not be routinely offered to patients with acute heart failure due to potential increased morbidity.

In summary, acute management of heart failure involves a range of treatments depending on the patient’s specific condition. It is important to carefully consider the potential side-effects and contraindications of each treatment, and to continue regular medication for heart failure where appropriate. Opiates should be used with caution, and only in cases where they are likely to reduce dyspnoea/distress without causing harm. With appropriate management, patients with acute heart failure can receive the care they need to improve their outcomes and quality of life.

A dry cough is a common side effect experienced by patients who begin taking an ACE inhibitor. However, in this case, the patient has been suffering from this symptom for four weeks and it is affecting her sleep. Therefore, it is advisable to switch her to an angiotensin II receptor blocker.

Angiotensin II receptor blockers are a type of medication that is commonly used when patients cannot tolerate ACE inhibitors due to the development of a cough. Examples of these blockers include candesartan, losartan, and irbesartan. However, caution should be exercised when using them in patients with renovascular disease. Side-effects may include hypotension and hyperkalaemia.

The mechanism of action for angiotensin II receptor blockers is to block the effects of angiotensin II at the AT1 receptor. These blockers have been shown to reduce the progression of renal disease in patients with diabetic nephropathy. Additionally, there is evidence to suggest that losartan can reduce the mortality rates associated with CVA and IHD in hypertensive patients.

Overall, angiotensin II receptor blockers are a viable alternative to ACE inhibitors for patients who cannot tolerate the latter. They have a proven track record of reducing the progression of renal disease and improving mortality rates in hypertensive patients. However, as with any medication, caution should be exercised when using them in patients with certain medical conditions.

Understanding Myasthenia Gravis: Symptoms, Diagnosis, and Treatment

Myasthenia gravis (MG) is a neuromuscular disorder that occurs when the body produces autoantibodies against the nicotinic acetylcholine receptor at the neuromuscular junction. This results in muscular weakness that is characterized by fatigability, meaning that the muscles become increasingly weaker during their use. MG primarily affects the muscles of the face, the extrinsic ocular muscles (causing diplopia), and the muscles involved in deglutition. Respiratory and proximal lower limb muscles may also be involved early in the disease, which can cause breathlessness and even sudden death.

Diagnosing MG can be challenging, as weakness may not be apparent on a single examination. However, electrodiagnostic tests and detecting the autoantibodies can confirm the diagnosis. The Tensilon test, which involves injecting edrophonium chloride to reverse the symptoms of MG, is now used only when other tests are negative and clinical suspicion of MG is still high.

Treatment of MG involves anticholinesterase medications, but many patients also benefit from thymectomy. It is important to note that a thymoma may be present in up to 15% of patients with MG.

Other conditions, such as transient ischaemic attacks, angina, multiple sclerosis, and somatisation disorder, may cause weakness, but they do not typically present with the same symptoms as MG. Therefore, it is crucial to consider MG as a potential diagnosis when a patient presents with fatigable muscular weakness.

If an adult with asthma is not able to control their symptoms with a short-acting beta agonist (SABA), the next step in their treatment plan should be to add a low-dose inhaled corticosteroid (ICS). This approach follows the guidelines set out by NICE for managing asthma.

The management of asthma in adults has been updated by NICE in 2017, following the 2016 BTS guidelines. One of the significant changes is in ‘step 3’, where patients on a SABA + ICS whose asthma is not well controlled should be offered a leukotriene receptor antagonist instead of a LABA. NICE does not follow the stepwise approach of the previous BTS guidelines, but to make the guidelines easier to follow, we have added our own steps. The steps range from newly-diagnosed asthma to SABA +/- LTRA + one of the following options, including increasing ICS to high-dose, a trial of an additional drug, or seeking advice from a healthcare professional with expertise in asthma. Maintenance and reliever therapy (MART) is a form of combined ICS and LABA treatment that is only available for ICS and LABA combinations in which the LABA has a fast-acting component. It should be noted that NICE does not recommend changing treatment in patients who have well-controlled asthma simply to adhere to the latest guidance. The definitions of what constitutes a low, moderate, or high-dose ICS have also changed, with <= 400 micrograms budesonide or equivalent being a low dose, 400 micrograms - 800 micrograms budesonide or equivalent being a moderate dose, and > 800 micrograms budesonide or equivalent being a high dose for adults.

If a lung abscess is not responding to intravenous antibiotics, percutaneous drainage should be considered as an option.

Correct: Arrange CT-guided percutaneous drainage. This is because the patient’s symptoms, such as swinging fevers, night sweats, pleuritic chest pain, dyspnoea, and cough, are consistent with a lung abscess. The chest x-ray also supports this diagnosis by showing a fluid-filled space within an area of consolidation. If IV antibiotics are not effective, percutaneous drainage can be guided by a CT scan or ultrasound. IV antibiotics may not be able to penetrate the abscess wall, which is why some patients do not respond to this treatment.

Incorrect: Arrange bronchoscopy. This is not commonly used for lung abscesses and is only indicated if an underlying tumour or foreign body is suspected. It is performed for diagnosis only, not drainage.

Incorrect: Arrange sputum cytology. Sputum cultures have already been collected, and a diagnosis of lung abscess has been established. This option could be considered later if the patient still does not respond to treatment to rule out an underlying malignancy.

Incorrect: Prescribe broad-spectrum IV antibiotics. This option is unlikely to be effective since the patient has already received IV antibiotics without success. The next step would be to manually drain the abscess.

Understanding Lung Abscess

A lung abscess is a localized infection that occurs within the lung tissue. It is commonly caused by aspiration pneumonia, which can be triggered by poor dental hygiene, reduced consciousness, or previous stroke. Other potential causes include haematogenous spread, direct extension, and bronchial obstruction. The infection is typically polymicrobial, with Staphylococcus aureus, Klebsiella pneumonia, and Pseudomonas aeruginosa being the most common monomicrobial causes.

The symptoms of lung abscess are similar to pneumonia, but they tend to develop more slowly over several weeks. Patients may experience fever, productive cough, foul-smelling sputum, chest pain, and dyspnea. Some may also have systemic features such as night sweats and weight loss, while a minority may experience haemoptysis. Physical examination may reveal dull percussion and bronchial breathing, as well as clubbing in some cases.

To diagnose lung abscess, a chest x-ray is usually performed, which shows a fluid-filled space within an area of consolidation. Sputum and blood cultures should also be obtained to identify the causative organism. Treatment typically involves intravenous antibiotics, but if the infection does not resolve, percutaneous drainage or surgical resection may be required in rare cases.

In most cases of pulmonary embolism, the chest x-ray appears normal.

Investigating Pulmonary Embolism: Key Features and Diagnostic Criteria

Pulmonary embolism (PE) can be challenging to diagnose as it can present with a wide range of cardiorespiratory symptoms and signs depending on its location and size. The PIOPED study in 2007 found that tachypnea, crackles, tachycardia, and fever were the most common clinical signs associated with PE. To aid in the diagnosis of PE, NICE updated their guidelines in 2020 to include the use of the pulmonary embolism rule-out criteria (PERC) and the 2-level PE Wells score. The PERC rule should be used when there is a low pre-test probability of PE, and a negative PERC result reduces the probability of PE to less than 2%. The 2-level PE Wells score should be performed if a PE is suspected, with a score of more than 4 points indicating a likely PE and a score of 4 points or less indicating an unlikely PE.

If a PE is likely, an immediate computed tomography pulmonary angiogram (CTPA) should be arranged, and interim therapeutic anticoagulation should be given if there is a delay in getting the CTPA. If a PE is unlikely, a D-dimer test should be arranged, and if positive, an immediate CTPA should be performed. The consensus view from the British Thoracic Society and NICE guidelines is that CTPA is the recommended initial lung-imaging modality for non-massive PE. However, V/Q scanning may be used initially if appropriate facilities exist, the chest x-ray is normal, and there is no significant symptomatic concurrent cardiopulmonary disease.

Other diagnostic tools include age-adjusted D-dimer levels, ECG, chest x-ray, V/Q scan, and CTPA. It is important to note that a chest x-ray is recommended for all patients to exclude other pathology, but it is typically normal in PE. While investigating PE, it is crucial to consider other differential diagnoses and to tailor the diagnostic approach to the individual patient’s clinical presentation and risk factors.

Treatment options for Mycoplasma pneumoniae infection

Mycoplasma pneumoniae is a bacterium that causes atypical pneumonia and is transmitted through respiratory droplets. The symptoms vary but can include fever, malaise, myalgia, headache, and a rash. Diagnosis is usually confirmed with serology, and treatment typically involves a macrolide antibiotic such as clarithromycin for at least 10-14 days. Penicillin and other beta-lactam antibiotics are ineffective as Mycoplasma pneumoniae lacks a cell wall. Tetracycline can be used but macrolides are preferred due to a better side-effect profile. Rifampicin is mostly limited to the treatment of tuberculosis and leprosy, while co-trimoxazole is not indicated for Mycoplasma pneumoniae infection. Extrapulmonary involvement is possible and may suggest the diagnosis in a patient presenting with pneumonia. A chest radiograph is non-specific and typically shows a reticulonodular or patchy consolidation pattern.

For patients with severe left ventricular dysfunction who are experiencing potentially reversible cardiogenic shock with hypotension, inotropic support on the high dependency unit (HDU) should be considered. This is because diuresis, which is the primary aim of management in acute pulmonary oedema, could lower blood pressure further and worsen the shock. Inotropes can help increase cardiac contractility and support blood pressure while diuresis is ongoing.

Biphasic positive airway pressure (BiPAP) is not an immediate consideration for this patient as it is used primarily for non-invasive ventilation in hypoxic and hypercapnic patients. Pulmonary oedema does not typically lead to hypercapnia.

Giving IV fluid for hypotension would not be appropriate as the hypotension is secondary to cardiogenic shock, not hypovolaemic shock. Administering further fluid in this scenario would worsen the patient’s condition by contributing to fluid overload.

Bisoprolol is contraindicated in this scenario as it suppresses the compensatory tachycardia that occurs in acute heart failure to maintain cardiac output, which would worsen the cardiogenic shock. However, outside of an acute scenario, a patient can continue on their routine bisoprolol if they are already prescribed this for heart failure, unless they are bradycardic.

Heart failure requires acute management, with recommended treatments for all patients including IV loop diuretics such as furosemide or bumetanide. Oxygen may also be necessary, with guidelines suggesting oxygen saturations be kept at 94-98%. Vasodilators such as nitrates should not be routinely given to all patients, but may have a role in cases of concomitant myocardial ischaemia, severe hypertension, or regurgitant aortic or mitral valve disease. However, hypotension is a major side-effect/contraindication. Patients with respiratory failure may require CPAP, while those with hypotension or cardiogenic shock may require inotropic agents like dobutamine or vasopressor agents like norepinephrine. Mechanical circulatory assistance such as intra-aortic balloon counterpulsation or ventricular assist devices may also be necessary. Regular medication for heart failure should be continued, with beta-blockers only stopped in certain circumstances. Opiates should not be routinely offered to patients with acute heart failure due to potential increased morbidity.

In summary, acute management of heart failure involves a range of treatments depending on the patient’s specific condition. It is important to carefully consider the potential side-effects and contraindications of each treatment, and to continue regular medication for heart failure where appropriate. Opiates should be used with caution, and only in cases where they are likely to reduce dyspnoea/distress without causing harm. With appropriate management, patients with acute heart failure can receive the care they need to improve their outcomes and quality of life.

Cavitating lung lesions can be caused by various factors, including infections and malignancies. In this case, the absence of a smoking history makes small cell and squamous cell lung cancers less likely. Small cell lung cancers typically affect the hilar or peri-hilar areas, while squamous cell lung cancers may present with pulmonary symptoms or paraneoplastic syndromes.

An aspergilloma is a fungal ball that forms in an existing lung cavity, often caused by conditions such as tuberculosis, lung cancer, or cystic fibrosis. While it may not cause any symptoms, it can lead to coughing and severe haemoptysis (coughing up blood). Diagnosis can be made through a chest x-ray, which will show a rounded opacity with a possible crescent sign, as well as high levels of Aspergillus precipitins. In some cases, a CT scan may also be necessary to confirm the presence of the aspergilloma.