This essay considers the pathophysiology, management and psychosocial aspects of a lower respiratory tract infection in the patient with chronic obstructive pulmonary disease (COPD). These are discussed in relation to a case study, with details obtained through interviews with the patient, and from her medical records.
DK is a 66 year old lady with COPD who presented to the A&E complaining of shortness of breath (SOB) at rest. She had a two-day history of worsening SOB and a cough producing yellow sputum. Her exercise tolerance was decreased from >1mile on the flat, to feeling unable to walk even a few yards. Her husband had recently had an upper respiratory tract infection. She had not experienced chest pain, ankle swelling, haemoptysis or weight loss and had not been recently hospitalised.
DK’s medical history includes hypertension, repair of dupytrens contracture, appendectomy, hysterectomy, tonsillectomy, and adenoid removal. Her drug history includes salbutamol inhaler, tiotropium, furosemide, ramipril, and quinine sulphate. She has no known drug allergies.
DK lives in her own home with her husband; she is normally independent and walks unaided. DK smokes 20 cigarettes daily, and has an estimated 40 pack-year smoking history. She does not drink alcohol.
On examination, DK’s airways were patent, and a widespread wheeze and bronchial breathing were audible on auscultation. Heart sounds were quiet, but normal. DK’s abdomen was soft and non-tender, bowel sounds were present. Her neurology was grossly intact. There was no ankle oedema or calf tenderness.
DK’s ECG had a poor trace, but showed sinus tacchycardia. A chest X-ray (CXR) showed right lower lobe consolidation. DK was on 60% oxygen (8L) oxygen. Arterial blood gas (ABG) measurements showed pH of 7.265, PO2 of 10.5kPa, PCO2 of 8.92, HCO3- 29.4. DK was put on 28% (2L) oxygen via a venture mask resulting in pH 7.306, pO2 8.05kPa, pCO 2 7.84kPa, HCO3- 28.6.
DK’s diagnosis was acute exacerbation of COPD, with type II respiratory failure, and respiratory acidosis. She was given 1L of saline (100ml/h), salbutamol (5mg neb) with hydrocortisone (200mg IV), and amoxicillin (500mg IV). DK was advised to stop smoking.
DK moved to AMU. She was alert, pain free, apyrexical and well on 28% oxygen. BP was 120/60, HR 110, and RR15.
The next day DK’s ABG’s on 28%O2 were pH 7.347, pO2 10.6, pCO2 7.27, HCO3- 24.1. The amoxicillin was stopped, and doxycycline (200mgOD) and prednisolone (30mgOD) started. She remained on 1L oxygen.
During the next two days DK’s monitoring and treatment continued. Her symptoms did not improve significantly, and she remained hypoxic. (pH: 7.452, PO2: 7.10, PCO2: 7.95, K+:3). Oxygen was changed to 3L
The following day, DK was still in respiratory failure (pH: 7.452, PO2: 7.10, PCO2: 7.95). Her potassium level was low (K+:3). She was continued on 3L O2, and K+ was replaced. DK was swiched onto IV Tazocin, and a CXR repeated.
The following day, DK was started on IV aminophylline. Antibiotics were continued. DK also discussed non-invasive ventilation, decided against intubation, and signed a DNAR.
Over the next few days DK’s symptoms resolved gradually, and she was discharged 5 days later.
COPD is a progressive disorder where the normal age related lung function decline is accelerated by intrinsic airway abnormalities, usually caused by smoking1. It is characterised by expiratory airflow obstruction (measured as FEV1<80% predicted, FEV1/FVC 0.72) not fully reversible with bronchodilators. Emphysema and chronic bronchitis are present together in 80% of cases, as in DK3.
Emphysema is defined histologically: abnormal permanent enlargement of the acini (airspaces distal to the terminal bronchioles), and septal destruction in the absence of obvious fibrosis4.p485. Emphysema is classified anatomically. Centriacinar is the most common type, and occurs in the upper zones, seen in DK as reduced vascular markings in the apical regions on CXR.
Chronic bronchitis is defined clinically as cough and sputum production on most days for three months for two consecutive years2. DK described such a cough. Effects in the medium sized bronchi (2-4mm) include increased luminal mucus secretion, goblet cell hyperplasia on a background of epithelial atrophy, squamous metaplasia, and ciliary abnormalities. The mucosa, smooth muscle, and submucosal glands are inflamed, and some smooth muscle hypertrophy occurs5.
In 90% of cases, COPD is caused by smoking3. Her smoking history suggests this is the case with DK. The mechanisms underlying COPD are not clearly defined; however several identified pathways lead to chronic bronchitis and emphysema. The most important are protease-antiprotease imbalance, and oxidative stress (Fig A).
COPD’s pattern is fixed airflow obstruction with little reversibility. The main airway obstruction mechanisms are mucociliary dysfunction, inflammation, and structural changes.
Submucosal gland hypertrophy and increased numbers of goblet cells result in mucus hypersecretion; squamous metaplasia causes ciliary dysfunction. Mucus plugs form in the small bronchii (<2mm)6.
In small airways, alveolar elasticity maintains patency. Alveolar damage in emphysematous lungs (DK’s), decreases airway elasticity and radial traction, increasing the lung’s compliance and ease of filling. On expiration, the airways collapse before expiration is complete, trapping air within the lungs1.
DK’s CXR shows evidence of chronic obstruction7.p168. Her lungs appear hyper-translucent and hyper-inflated (8 posterior ribs visible, normal <7). The hemi-diaphragms are flat. Collapsed airways generate the polyphonic wheeze heard throughout expiration over both of DK’s lung fields. DK was expiring through pursed lips, a compensatory mechanism, causing back pressure holding the airways open, improving air expulsion.
Ventilation Perfusion (V/Q) Mismatch
V/Q mismatch in COPD occurs because well perfused lung is poorly ventilated due to air remaining in the alveoli after expiration. Enlarged distal airspaces decrease surface area for diffusion, limiting gas exchange. Poorly ventilated lung will not have the required diffusion gradient for effective transfer of CO2 out of the blood, and O2 in. Blood leaving these areas will have relatively high PCO2 and low PO2. Deoxygenated blood mixes with oxygenated blood from ventilated areas causing a venous admixture. In chronic bronchitis this is more marked than in emphysema in which the inflammatory processes and alveolar scarring and fibrosis also damage the vasculature. Type II failure is more likely in a patient like DK with chronic bronchitis.
In acute COPD exacerbation, the patient’s symptoms worsen abruptly, often including purulent sputum production8. DK’s increased SOB, worsened productive cough, and visible consolidation on her CXR indicate an infective exacerbation cause7.p426. Bacterial infection is the most common cause of exacerbations (50%)9. The pathogenesis is outlined in figure B.
Infection occurs either by new colonisation of the lungs with pathogenic bacteria, or more commonly by strain mutation, or viral co-infection. Viral infection allows better infiltration of bacteria into the lung epithelium in a complex synergistic relationship10.
COPD patients’ lungs mucociliary and innate cellular defences are impaired, and they have less respiratory reserve. They are more prone to infection, and less able to cope during infection.
Bacterial infiltration activates alveolar neutrophils. These recruit elastase, activating alveolar macrophages. This activates circulating neutrophils, which leave the circulation and are recruited, damaging interstitium, and increasing elastase production in a positive feedback loop. Increased vascular permeability causes fluid to leak into the alveoli. Î±1 antitrypsin inhibits elastase activity and slows recruitment in a negative feedback control system.
Alveolar macrophages secrete cytokines activating fibroblasts, and bacterial cell walls secrete chemoattractants (FMLP) and activate complements, summoning more inflammatory cells. Alveoli become packed with neutrophils and monocytes, and ventilation of a lung region is lost, causing further V/Q mismatch. When patients become symptomatic, antibiotic intervention, and coughing which clears mucus full of cells infiltrated by inflammatory cells, may end the process. Otherwise, hepatisation develops leading to fibrosis. Resolution occurs when apoptosis causes lymphocytes to leave the alveoli, or death occurs from respiratory failure11.
In respiratory failure, the lungs inadequately exchange gas, and fail to maintain PaO2 and PaCO2 within the normal range. There are two types of respiratory failure. Type I is low PO2 <8.0kPa, with normal or low PCO2 â‰¤6kPa. Type II is low PO2<8kPa, and raised PCO2 >6kPa12.
On presentation, DK was in type II respiratory failure. Her PO2 On 60% oxygen was artificially high at 10.5kPa and PCO2 was 8.92kPa. DK probably has a degree of chronic hypercapnia. This produces a mild acidosis, effectively compensated by a metabolic alkalosis. During exacerbation, increased VQ mismatch causes PCO2 to increase. Compensatory mechanisms may be overcome, producing a respiratory acidosis, as in DK. Long term hypercapnia reduces CO2 sensitivity; therefore, respiration is maintained by hypoxic drive.
COPD exacerbation management has three main components: drug therapy, supportive therapy, and lifestyle modification13. DK’s drug therapy will be aim to improve symptoms and treating her pulmonary infection. Supportive therapy will help manage DK’s respiratory failure and improve lung function. Smoking cessation will be encouraged. DK’s long term management must be assessed, to prevent or minimize future exacerbations. DK’s management was consistent with British Thoracic Society and NICE consensus guidelines14.
Upon acute COPD exacerbation diagnosis, DK was assessed as requiring hospitalisation rather than community management. Based on her rapidly deteriorating condition, poor mobility, and type II respiratory failure, DK was admitted14. There were no recorded spirometry results. Although not essential for diagnosis, FEV1 could have been useful to assess exacerbation severity. FEV1<1L is considered severe15.
During her hospitalisation, DK continued her regular medications: salbutamol inhaler, tiotropium, furosemide, ramipril, and quinine sulphate.
Oxygen therapy is important in managing COPD exacerbation as it reduces mortality and shortens hospitalisation16.
Hospital oxygen therapy aims to maintain the patient’s oxygen saturation at a target value. Targets defined for each patient are generally 88%-92%, balancing hypoxia, hypercapnia, and pH7. DK’s target in hospital was 88%. This value was chosen rather than a higher one because DK may have long-term type II respiratory failure, with chronic hypercapnia, and may rely on hypoxic drive to maintain breathing. High oxygen concentrations can remove this hypoxic drive, and depress respiration. It is therefore important to assess patients immediately before oxygen therapy where possible, with blood gas analysis the preferred measure17.
DK’s case illustrates this danger. On 60%ambulatory oxygen, DK’s PaCO2 was 8.92kPa, and pH was 7.265. When changed to 28% oxygen, although DK’s PaO2 decreased from 10.5kPa to 8.05kPa, her PaCO2 decreased to 7.84kPa, and pH increased to 7.306. High carbon dioxide concentrations are toxic. At 8-10kPa, patients experience severe dyspnoea. Above 10.5kPa patients can become lethargic or semi-comatose, and above 16kPa, anaesthesia, respiratory depression, and ultimately death can occur6. High carbon dioxide concentrations also result in respiratory acidosis (CO2+H2O ƒ H2CO3).
During her stay, DK’s blood gasses were monitored regularly, and oxygen therapy adjusted accordingly because respiratory failure in DK’s exacerbation is caused by the infection. Her oxygen needs will change along the course of the exacerbation.
Non invasive positive pressure ventilation (NIPPV) allows improved air entry. NIPPV improves survival and reduces complications in COPD exacerbation18. This was discussed with DK as a treatment option. She agreed to use it if necessary, but decided that she would not want intubation. DK signed a DNAR.
In A&E, DK also received nebulised salbutamol (5mg). Salbutamol is a short-acting bronchodilator that works by agonising Î²2 receptors. This initiates a second messenger cascade, increasing intracellular cAMP and activating protein kinase. This causes phosphorylation and inhibition of myosin-light-chain-kinase, leading to smooth muscle relaxation. Salbutamol also increase mucus clearance by cilia, and can inhibit release of several inflammatory cytokines19. This reduces obstruction, and improves symptoms7.
The best method of administering a therapeutic dose to DK quickly was via a nebuliser driven with compressed air as opposed to oxygen in view of her respiratory failure. Oxygen therapy can continue via nasal cannulae if required16p.98.
Salbutamol is not selective for Î²2, and has the potential to cause fine tremor, nervous tension, and tachycardia if it agonises Î²1 receptors, significantly cardiac. These effects are unlikely at inhaled doses in the amount used for bronchodilation19. Salbutamol is effective only for 3-5 hours, and so tends to be prescribed, as for DK, on an as needed basis20.
DK continued to take tiotropium, a long acting bronchodilator. Tiotropium antagonises M3 muscarinic receptors, inhibiting smooth muscle contraction and mucus secretion, causing bronchodilation19.
On day five of her admission, DK was started on IV aminophylline. Aminophylline, a xanthine drug, acts as a bronchodilator with an unknown action mechanism. It is thought to inhibit phosphodiesterase isoenzymes, causing increased cAMP and cGMP, leading to smooth muscle relaxation. Adenosine receptor antagonisms and anti-inflammatory effects are also possible mechanisms. The evidence supporting its use in COPD is limited. NICE recommends it when response to nebulised bronchodilators is unsatisfactory. Risks of theophylline therapy are significant, with side effects common at doses greater than 110Î¼mol/l. Above 200Î¼mol/l, serious CNS and cardiovascular effects occur. The therapeutic index is therefore very narrow19. Due to these risks, DK’s theophylline levels were carefully monitored.
DK also received in A&E intravenous hydrocortisone (200mg) stat dose. She was then started on oral prednisolone (30mg OD) for 5/10 days. Hydrocortisone and prednisolone are glucocorticosteroids. These suppress inflammation by decreasing the activity and influx of leukocytes, decreasing T cell and B cell clonal expansion, and inhibiting T cell cytokine secretion. Hydrocortisone also upregulates Î²2 receptors, improving the effect of bronchodilators19. Corticosteroids shorten hospitalisation, and hasten lung function improvement21.
Oral corticosteroids have wide-ranging and significant side effects and should not be used long term. Side effects are less common with inhaled steroids, but there is no evidence of inhaled steroid effectiveness in acute COPD exacerbations16.
DK’s CXR showed consolidation, and she was producing yellow sputum. These signs indicate pneumonia. She was therefore immediately started on IV amoxicillin (500mg). Amoxicillin is a broad spectrum bactericidal Î² lactam antibiotic. It is the first-line antibiotic for treating infective COPD exacerbation14 because it is effective against Haemophilus influenzae, Streptococcus pneumoniae, or Moraxella catarrhalis, and Mycoplasma pneumoniae22,23, the most common pathogens implicated in exacerbations. Amoxicillin binds to penicillin-binding proteins on the bacteria, inhibiting the transpeptidases involved in cross-linking peptide chains on the peptidoglycan. Inhibition of a cell wall autolysis inhibitor results in bacterial destruction19.
The day after admission, the respiratory team took over DK’s care. Amoxicillin was stopped and doxycycline (200mgOD) started. Doxycycline is a tricyclic antibiotic and is another first-line treatment of infective exacerbation. Doxycycline is a very broad spectrum tetracycline antibiotic, and is more effective against the organisms that cause infective exacerbations. It is actively transported into susceptible bacteria where it inhibits tRNA binding, preventing protein synthesis. This is a bacteriostatic drug; it inhibits the growth and reproduction of bacteria, but does not kill them19.
Four days later, DK was not showing signs of improvement. One possible reason was bacterial resistance to the antibiotics. Resistance occurs by six mechanisms (fig C).
Tazocin was substituted for doxycycline to target resistant, Î² lactamase producing bacteria. Tazocin consists of piperacillin with tazobactam20. Piperacillin is another broad spectrum Î² lactam antibiotic that acts similarly to amoxicillin. Tazobactam is a drug that binds irreversibly to and inhibits plasmid- and chromosome-mediated Î²-lactamases. This prevents bacteria from deactivating the antibiotic. This increases the effective range of piperacillin19. A CXR was repeated to assess pulmonary infection progression, help guide management, and ensure that no other lung pathology had been missed7. This CXR still showed consolidation in the lower lobes, indicating persistent infection.
Over the next few days, DK was monitored. Her condition improved gradually, and she was discharged 5 days later.
Psychological and Social Aspects
Expanding tobacco use worldwide is increasing COPD prevalence24. COPD exacerbation accounts for about 2.4% of acute admissions25. Exacerbation is a significant cause of mortality, (8% die whilst in hospital, 14% do not survive 3 months from admission, and 23% do not survive 1 year25,26. Mortality increases for patients like DK with type II respiratory failure (20% at 60 days, 47% at 1 year, and 49% at 2 years)27.
COPD exacerbations often require recurrent hospitalisation (34% readmission rate within 3 months)28 diminishing quality of life. The majority of exacerbations are community managed. Statistics mask the full social burden because about 50% of cases are unreported25. COPD is projected to become the fifth ranking cause of lost DALYs by 202024.
Exacerbation incidence increases with COPD severity. Severe sufferers average 3.43 exacerbations annually, compared to 2.68 for moderate sufferers. Exacerbations increase with age29, and are 50% more common in winter25. The leading exacerbation cause is infection, accounting for 50-70% of cases. Viruses are implicated in approximately 20% of cases; 30% are of unknown aetiology26.
Smoking is the most significant COPD risk factor; continued smoking is an exacerbation risk factor. Lifestyle modification and pharmacological intervention help prevent COPD. Appropriate COPD management reduces morbidity, mortality, hospital admission, and cost. COPD directly costs the NHS an estimated £492 million annually; estimated indirect costs are £981 million30.
Smoking and Cessation
Government smoking prevention initiatives include banning tobacco advertising and promotion, health warnings on tobacco, banning indoor public smoking, anti-smoking advertising, and health promotion campaigns.
Smoking cessation is beneficial at any disease stage, improving lung function (FEV1) and reducing exacerbation risk 25. For DK, smoking cessation will impact disease progression. Impediments include reluctance to quit, and family member influence. DK expressed a desire to stop, and reduced her smoking in hospital. However, DK’s husband also smoked.
Encouraging cessation should be routine COPD management31. Non-judgmental behavioural support, nicotine replacement therapy, and other drug therapies can help. Advice is available from the NHS smokefree website32. Although DK was advised to stop smoking, more information could have been provided about pharmacological and behavioural interventions.
Exacerbations can cause patients like DK to further lose function and experience severe, distressing symptoms. Upon presentation, DK’s dyspnoea had reduced her mobility and exercise tolerance, making daily tasks difficult. Symptom management supports quality of life, and is associated with improved psychological comfort. Dyspnoea is strongly linked to anxiety, with suggested common pathophysiology33. Dyspnoea and anxiety can form a ‘vicious cycle of breathlessness’ preventable by effective management16.p142. In addition to physiotherapy and bronchodilators, long-term home oxygen therapy helps correct hypoxaemia and breathlessness. It would be beneficial for DK, but smokers are ineligible for home oxygen.
Influenza and pneumococcal vaccination have been shown to reduce exacerbations, as have pulmonary rehabilitation, long-acting bronchodilators, and inhaled corticosteroids16.
Anxiety and Depression
Patients’ adaptability and perception of their condition can impact quality of life more than the disease itself16. COPD patients confront physical and lifestyle changes, changes in social position, poor mobility, and dependency. These can result in social isolation and physical deterioration. Anxiety and depression, common in COPD patients, are associated with morbidity, functional impairment, and mortality33,34. 42-57% of COPD patients suffer from depression33. Key factors associated with anxiety and depression are gender (47% of females vs. 34% of males)35, repeated exacerbation33, and continued smoking35. All of these apply to DK, who is at high risk for anxiety and depression. Psychological assessment should be an important part of DK’s management16. Effective management of psychiatric issues can improve psychological function and lung function33. 82% of patients suffering from depression or low mood report that no intervention was offered.
Family and Social Support
Strong family and social networks positively impact quality of life and health outcome16. DK’s husband was at her bedside almost constantly. Community support is also important. British Lung Foundation groups36 and an NHS blog37, enable patients to discuss issues with others. A holistic approach will strengthen DK’s psychosocial wellbeing, and reduce prospects of future hospitalisation.
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