An Overview of Physiotherapy in UK Prisons

Original Editor - Andrea Beznaczuk-Smyrnew, Mark Chawke, Niamh Coveney, Anthony Gorsek, Jo Hampton, Katie McGregor as part of the QMU Current and Emerging Roles in Physiotherapy Practice Project

Top Contributors - Andrea Beznaczuk-Smyrnew, Anthony Gorsek, Mark Chawke, Kim Jackson, Katie McGregor, Niamh Coveney, Admin, Jo Hampton, George Prudden, WikiSysop, Vidya Acharya, Olajumoke Ogunleye and 127.0.0.1  

 

 Chronic Obstructive Pulmonary Disease 

Chronic obstructive pulmonary disease, or COPD, is an umbrella term often used to define various conditions. Two of the most common conditions include chronic bronchitis and emphysema, which are characterised as a difficulty in breathing due to permanent damage to the lungs. Other diseases that contribute to COPD are obstructive bronchiolitis, pulmonary vascular disease, cor pulmonale (right sided heart failure and pulmonary heart disease), and systemic syndrome of cachexia and muscle weakness. While the damage on the lungs is non-reversible, it is a preventable and treatable condition (Kon et al. 2011). It is the most prevalent cause for morbidity and mortality worldwide and subsequently places a heavy economic and social burden on governments (Celli et al. 2004). (Go to politics) – The prevalence of COPD’s effect on economy is greatly underestimated due to its consequential late diagnosis, because people who present with moderate or severe symptoms. Onset of the disease can occur as early as 40 years old; however, it more commonly seen in individuals over the age of 65. Several factors, including late diagnosis and socioeconomic factors, are responsible for this varying age in diagnosis.

Pathophysiology
COPD effects four compartments of the lungs – central airway, peripheral airway, lung parenchyma, and pulmonary vasculature. The common risk factors (listed below) cause an inflammatory response in these areas leading to pathological lesions in COPD sufferers.  Additionally, the lungs are susceptible to an imbalance of proteinases and antiproteinases, and oxidative stress, causing the following physiological defects:

• Mucous hypersecretion
• Cilliary dysfunction
• Airflow limitation and hyperinflation
• Gas exchange abnormalities
• Pulmonary hypertension
• Systemic effects

Smoking, the leading cause of COPD, has been estimated to contain 1017 reactive oxidant species (ROS). ROS instigate a wide range of inflammatory, mucosecretory, proteolytic, and fibrotic responses, which consequently cause the release of chemotactic factors and cytokines due to epithelial cell injury and macrophage activation. Macrophage and neutrophil involvement cause the breakdown of the extracellular matrix, which corresponds with an inflammatory response. Pathologically, an increase in cigarette smoke parallels a greater number of inflammatory and repair (fibrosis as a consequence) cycles on these response systems (Kon et al. 2011), which commonly manifests as mucus hypersecretion, fibrosis, proteolysis, and airway and parenchymal remodelling (Kon et al 2011) .

Causes of COPD
Characterised by a progressive reduction in airflow resulting in an atypical inflammatory lung response to carcinogenic particles or gases, COPD is a preventable and treatable disease state. Smoking is the leading cause of COPD, however other factors, such as air pollution, environmental factors, and genetics factors, can also be precursors to the development of COPD.
1. Smoking: the most common cause of COPD. It has been estimated that cigarette smoke can contain over 1000 reactive oxidant species (ROS) (Kon et al. 2011). Smoking cessation can gradually reduce your risk of getting COPD, or slow its progression if diagnosed in the earlier stages of the disease.
2. Air pollution, environmental factors: toxic fumes, chemicals (e.g. smoke inhalation from biomass fuel, predominantly in developing countries) (Kon et al. 2011 – global burden)
3. Alpha-1-antitrypsin (A1A): genetic condition where individuals are A1A deficient, or produce low levels, of a protein produced by the liver and found in the blood. Its role is to protect lung tissues from being degraded by surrounding enzymes. COPD and symptoms can be further exacerbated with A1A deficiency and smoking.

Diagnosis
Diagnosis of COPD requires the use of spirometry, which measures the amount of air expelled from the lungs in the first seconds of expiration. If the FEV1/FVC ratio is ≤ 0.70, then the bronchial tubes are narrowed, or damaged, to an extent where an individual experiences common symptoms (listed below) of COPD
Symptoms:
• Cough
• Excessive sputum production
• Dyspnoea (breathlessness; ranked on a scale of 0 to 4, where 0 = not troubled with breathlessness except with strenuous exercise and 4 = too breathless to leave the house, or breathless when dressing/undressing)
• Exposure to risk factors
The use of spirometry has been documented as being a useful tool for predicting an individual’s health status, utilisation of healthcare resources, the development of exacerbations, and mortality (Celli et al. 2004). Spirotmetry is also readily used to track the progress of the disease and establish an appropriate course of treatment (ScotPHO, 2013).
Extrapulmonary systemic symptoms:
• Muscle weakness and wasting
• Cachexia
• Cardiovascular disease
• Metabolic syndrome (i.e. diabetes, obesity, high BP)
• Endocrine effects
• Anaemia
• Depression
• Malignancies

 Treatment

Smoking Cessation

Antibiotics
1. Corticosteroids
2. Respiratory stimulants
3. Diurectics
4. Anticoagulants

Physiotherapy and COPD
Various physiotherapy techniques have been well-documented as having appositive effect on symptoms experienced by COPD patients.

References

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