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Case StudyIntroductionThis case study describes a sixty-year-old male with a significant smoking history (up to 35 cigarettes a day) presenting with complaints of worsening shortness of breath, exercise intolerance, and a productive chronic cough, with occasional blood-streaked sputum. He also recal...

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Case Study

Introduction This case study describes a sixty-year-old male with a significant smoking history (up to 35 cigarettes a day) presenting with complaints of worsening shortness of breath, exercise intolerance, and a productive chronic cough, with occasional blood-streaked sputum. He also recalls frequent exacerbations of his cough and shortness of breath over the past 15 years. During general physical examination, notable observations included bluish discolouration of the skin, visible engorgement of neck veins, and bilateral pitting oedema of the lower limbs. On palpation, the patient’s liver was also moderately enlarged. Auscultation revealed bilateral coarse crackles with a prolonged expiratory phase and added cardiac sounds. The analysis will describe all the possible pathophysiological pathways of the patient's presentation, while also highlighting close differential diagnoses. An evidence-based review of diagnostic tests is also included.

Pathophysiology of Patient's Complaints

Dyspnoea Progress shortness of breath; otherwise known as progressive dyspnoea, was one of the significant presenting complaints of the patient described. Dyspnoea is a common symptom reported in conditions such as asthma, bronchiectasis, and chronic obstructive pulmonary disease (COPD) and is described simply as the uncomfortable sensation produced when there is a mismatch between oxygen delivery and demand (Anzueto & Miravitlles, 2017). Dyspnoea results from multiple pathophysiological pathways (Anzueto & Miravitlles, 2017). These pathways include airway narrowing, lung hyperinflation, impaired gaseous exchange, mucus hypersecretion, and neuromechanical dissociation (Antoniu, 2010). Repeated inflammatory responses to noxious stimuli such as cigarette smoke, lead to chronic inflammation, resulting in fibrosis (Suthahar et al., 2017). Fibrosis is the replacement of

functional lung and airway tissue with non-functional scar tissue. Accumulation of this scar tissue leads to the narrowing of the airway, subsequently impeding the flow of air, most importantly oxygen, to the respiratory alveoli. The chronic narrowing of airways is a feature common to COPD and asthma, that contributes to dyspnoea in these conditions (Bosch et al., 2021). Asthma, an allergic reaction to specific antigens such as pollen, is characterised by the reversible spasm of airways, particularly medium-sized bronchioles, due to the degranulation of inflammatory mediators (Abbas et al., 2021). The acute narrowing of airways leading to dyspnoea is unique only to asthma. Patients with a tendency for asthmatic attacks have increased quantities of circulating immunoglobulin E (IgE) in their bloodstream that bind to mast cells, triggering a hypersensitivity reaction on exposure to antigens. Mucus hypersecretion is also a feature of asthma due to mast cells' degranulation, which leads to a chronic cough (Martínez-Rivera et al., 2018). The accumulation of mucus reduces the area for air to move through. Furthermore, repeated acute inflammatory responses and infections also damage the cells lining the alveoli, reducing oxygen absorption from the lungs into the blood vessels (Goldklang & Stockley, 2016). Alpha-1 antitrypsin deficiency and bronchiectasis are conditions with a genetic predilection to infections that can cause progressively worsening shortness of breath due to damage to the lung’s epithelial lining (Meseeha & Attia, 2021). Additionally, excessive mucus production is one of the critical pathophysiological features of bronchiectasis (Bird & Memon, 2021). Emphysema, a histopathological variant of COPD, is characterised by damage to the alveolar epithelium reducing the surface area for oxygen absorption (Celli et al., 2018). All these factors combined limit oxygen delivery to blood vessels and, subsequently, body tissues. Dyspnoea is not only the result of decreased oxygen supply, as an increased oxygen demand also plays a crucial role. With the narrowing of the airways, increased quantities of air, known as dead space, accumulates in the air spaces (Intagliata et al., 2021). The dead space contains non-functional air that does not take part in the respiratory exchange but is necessary to prevent the lungs from collapsing. However, an increased dead space and an expanded lung also means that the lung muscles have to work against a greater resistance and recoil strength to expel gases such as carbon dioxide (Chen et al., 2016). This is known as an

increased work of breathing and represents an increased demand for oxygen by the body. The mismatch in oxygen demand and supply is further amplified due to physical activity, increasing oxygen demand (Boyette & Manna, 2021). This could account for the dyspnoea and light-headedness the patient experienced even during routine physical activities such as walking. The inability of the body, in particular the heart, to adequately supply essential organs and tissues with oxygenated blood can also result in dyspnoea. This can result from one of two pathways. First, the inadequate pumping ability of the heart, and second a localised blockage, for instance, a thrombus or emboli in the vessel supplying an organ or tissue (Berliner et al., 2016). Dyspnoea is also associated with anxiety and depression stemming from the limitations on physical activities (Matte et al., 2016). The depression, which is associated with overeating, coupled with the lack of physical activity, can account for the weight gain that the patient experienced.

Chronic Cough and Purulent Sputum In response to cigarette smoke, acute lung inflammation leads to goblet cell proliferation, leading to increased mucus production (Tian & Wen, 2015). Mucus is thick, phlegmatic material that traps foreign materials such as dust and bacteria and prevents them from reaching the alveoli. In normal circumstances, mucus is cleared by the upward beating motion of cilia and eventually swallowed (Tian & Wen, 2015). However, due to a prolonged inflammatory response to noxious stimuli, the amount of mucus produced far exceeds the capability of cilia to clear it. Furthermore, the lung inflammatory response also leads to the death of ciliated epithelium cells. Conditions like asthma and COPD, as discussed earlier, also result in the production of excess mucus. Chronic bronchitis, another histopathological variant of COPD, is a clinical diagnosis defined by the occurrence of productive cough for at least three months a year for two consecutive years, which shares much of it is pathophysiological pathways with COPD and emphysema (Dotan et al., 2019). Although chronic cough in this case has not been quantified, the patient highlights yearly exacerbations in cough and sputum intensity, which subsequently raises the possibility of chronic bronchitis as a potential diagnosis. Additionally, some genetic conditions, such as Kartagener syndrome,

a known cause of bronchiectasis, are typified by the absence of ciliary function, leading to mucus collection in the airways (Stern & Sharma, 2021). Accumulated mucus irritates the lung airways, leading to a productive chronic cough rich in sputum (Widysanto & Mathew, 2021). The collection of mucus resulting from the inflammatory response in conditions such as COPD, asthma, and bronchiectasis also serves as a focus for repeated infections accounting for the bi-yearly infections experienced by the patient in this case. The bacteria colonise the respiratory mucosa causing a range of infections with streptococcus pneumonia and pseudomonas, being the most active pathogens (Chai & Xu, 2020). As discussed, repeated infections cause damage to the lung parenchyma, further increasing the susceptibility to infections (Tian & Wen, 2015).

Haemoptysis Haemoptysis, i.e., blood-stained mucus, results from a fragile epithelium and chronic cough (Runggaldier et al., 2018). Respiratory infections and toxins, such as cigarette smoke, weaken the epithelium lining respiratory airways while forceful, repetitive cough erodes the already fragile and inflamed epithelium leading to the rupture of small blood vessels (Ittrich et al., 2017). Blood from these vessels mixes with the sputum, thus, producing a blood-tinged sputum. Since the patient is not experiencing any blood coagulation disorder, as evidenced by the normal laboratory findings and lack of corroborating history, and given the small size of the vessels damaged, the blood loss is not profuse. However, due to the persistent nature of the cough and a fragile epithelium, episodes of haemoptysis are likely to recur. Physical Examination Findings

Distended Neck Veins One of the essential examination findings in the case study presented is that of engorged neck veins, particularly the jugular vein. The main pathophysiological pathway responsible for jugular distention is the accumulation of blood in the jugular vein. This stems from either the inability of the heart to adequately pump blood or any obstruction in the cardiac outflow tracts (Omar & Guglin, 2018).

The inability of the heart, in particular the left side, results in the pooling of blood in the lungs, which in turn increases the vascular resistance that the right ventricle has to overcome (Ahmed, 2011). With time, the right ventricle weakens under the increased workload, and because the right side of the heart receives blood directly from the jugular veins via the subclavian and brachiocephalic vein, blood accumulates in these veins, causing them to distend. In extreme situations, this condition is also referred to as cardiogenic shock. Outflow obstructions resulting in jugular vein distention is rare; however, it may be seen in conditions such as malignancies of the lungs or superior vena syndrome (Straka et al., 2016).

Bluish Discolouration of Skin Cyanosis is the medical term for the bluish discolouration of the skin, which results from increased quantities of deoxygenated blood, owing to its blue colour, in circulation (Adeyinka & Kondamudi, 2021). Broadly, there are three reasons for cyanosis, first, the decreased oxygen-carrying capacity of the blood, second, the reduced supply of oxygen to lung alveoli, and lastly, obstruction in a blood vessel supplying the affected region. Red blood cells (RBCs) are the leading oxygen carriers in the blood (Helms et al., 2018). A deficiency of RBCs, termed anaemia, can be caused by several genetic, dietary, and vascular causes, which reduce the ability of blood to carry oxygen (Chaparro & Suchdev, 2019). The pathophysiological pathways responsible for decreased oxygen supply to lung alveoli and obstruction of blood vessels have already been discussed in the preceding sections.

Generalised Pitting Oedema Generalised pitting oedema is the accumulation of excess interstitial fluid in the dependent areas of the body, especially the lower limbs (Whiting & McCready, 2016). It results from the gross accumulation of blood in these areas, which in turn raises hydrostatic capillary pressure, forcing increased fluid into the interstitial compartment (Lent-Schochet & Jialal, 2021). Usually, excess interstitial fluid is drained away via lymphatic channels; however, excessive collection overwhelms these channels leading to the development of oedema. Thus, it is no surprise that the obstruction of lymphatic channels also results in the development of oedema. Other reasons for the development of oedema include loss of circulating protein, called albumin, which reduces colloid osmotic pressure and fluid movement into extracellular compartments (Lent-Schochet & Jialal, 2021).

The excess interstitial fluid does not solely accumulate in the lower limbs. It may also accumulate in the abdomen (ascites), the lungs (pleural effusion), and the heart (pericardial effusion) (Pedersen et al., 2015). Ascitic accumulation explains the abdominal distention this patient experienced.

Coarse Crackles Coarse crackles are additional lung sounds, generally heard during inspiration, produced by fluid accumulation in lung spaces. They are regarded as a sensitive physical examination finding of typical respiratory infections such as pneumonia and some cardiac conditions such as congestive heart failure (Sarkar et al., 2015). The accumulation of fluid in lung spaces secondary to infections is the result of an inflammatory reaction. Oedema is a tell-tale sign of inflammation resulting from localised vascular changes such as increased permeability and increased blood flow to affected regions (Heymann, 2019). The other causes of fluid accumulation have already been discussed. Significant Laboratory Findings

Elevated Haematocrit, Red Blood Cell Count, and Haemoglobin Level Haematocrit (HCT) is the ratio of RBCs to blood plasma volume and thus, is directly proportional to the RBC count and inversely proportional to plasma volume. Haemoglobin is the iron-containing pigment that makes up the RBC and is responsible for carrying oxygen. All the aforementioned values were elevated in the patient described in this case- HCT 57% (Normal range: 38.3- 48.6%), RBC count 6.8 x 1012/L (Normal range: 4.35- 5.65 x 1012/L) and haemoglobin level 200g/L (Normal range: 14-17 g/L) (Mondal & Budh, 2021). Hypoxia, i.e., reduced delivery of oxygen to metabolically active tissues, is the primary reason for the elevation in all the parameters listed. Hypoxia is detected by central and peripheral chemoreceptors, which in addition to making appropriate adjustments to rate and depth of respiration, stimulate the peritubular cells of the kidneys to release erythropoietin (Tojo et al., 2015). Erythropoietin is a hormone that stimulates the bone marrow to increase its production of RBCs. This serves as a compensation mechanism for decreased oxygen

delivery to metabolic tissues. The elevated RBC count, termed polycythaemia, as discussed raises the haematocrit and overall haemoglobin concentration. Another reason for the concurrent increase in the parameters is the relatively greater loss of blood plasma than RBCs. This can occur in acute blood loss, for instance following a vehicular accident (Cuthbert & Stein, 2019). However, the patient did not suffer any acute bleeding disorder and thus, this cannot be related to cause. Blood plasma may also be reduced due to decreased oncotic capillary pressure in conditions such as liver failure or an increase in hydrostatic capillary pressure in conditions such as heart failure (Giorgio et al., 2017).

Pulse Oximetry The pulse oximetry value is a measure of blood oxygen saturation level with a value of 95% and greater considered normal (Jubran, 2015). This patient had less than normal, i.e., 92%, oxygen saturation levels at room air. The two primary determinants of oxygen saturation levels, much like dyspnoea, are the supply of oxygen and the oxygen-carrying ability of the blood. As discussed previously, conditions such as COPD, emphysema, and asthma, just to name a few, limit the supply of oxygen to alveoli, leading to decreased blood saturation levels. Similarly, a decrease in haemoglobin and RBC counts limit blood oxygen-carrying ability, leading to a decrease in blood saturation levels.

White Blood Cell (WBC) Count and C-reactive Protein (CRP) Levels White blood cells, produced by the bone marrow, are the body's primary defence mechanism against foreign invaders such as bacteria (Miller et al., 2015). C- reactive protein is a pentameric protein synthesised by the liver (Nehring et al., 2021). Together, both these values are termed inflammatory markers and sensitive measures of acute inflammation and infection. Since the patient in this case is not suffering from an acute inflammatory or infectious process, both these values are within the normal range

Other Routine Blood Metrics Mean corpuscular volume (MCV), a measure of red blood cell volume, mean corpuscular haemoglobin concentration (MCHC), a measure of haemoglobin concentration per unit of blood, and mean corpuscular haemoglobin (MCH), which shows the amount of haemoglobin

in each RBC, are particularly useful metrics when making a diagnosis of anaemia (Chaparro & Suchdev, 2019). These metrics were normal in this patient therefore a diagnosis of anaemia was not suspected. Similarly, reticulocytosis, an indicator of bone marrow function, helps diagnose anaemia and leukemia, but for the aforementioned reasons, these tests, too, were normal in this patient (Meier et al., 2014). Abnormalities in platelet levels, the blood component responsible for clotting, indicate bone marrow health and serve as a potential marker for malignancies and acute infection (Qu et al., 2018). In the absence of these conditions, the platelet count was within normal limits in this patient.

Differential Diagnosis List

Chronic Obstructive Pulmonary Disease (COPD) Based on the patient's history of smoking, frequent bouts of infections, and the constellation of signs and symptoms described, the most likely diagnosis in this case is COPD. Exacerbations of COPD are defined by an increase in baseline levels of cough, sputum production, or dyspnoea and are a common complication in sufferers of COPD (Wheaton et al., 2019). The patients’ history provided a typical yearly pattern on COPD exacerbations, further increasing the likelihood of a COPD diagnosis. COPD is the third leading cause of death worldwide (Terzikhan et al., 2016). It is primarily a disease of the lungs and airways which is characterised by an abnormally exaggerated response of the lungs and its airways to noxious particles, gases, and immunogens, resulting in mucus hypersecretion, irreversible narrowing, and obstruction, in addition to the destruction of lung parenchyma (Olloquequi et al., 2018; O’Reilly, 2016). Prolonged smoking, which the patient in this case partook in, is the leading cause of COPD (Wheaton et al., 2019). This is because cigarette smoke contains a high concentration of oxidants which induce inflammation of the lungs and its airways (Eapen et al., 2017). Repetitive exposure to cigarette smoke leads to a prolonged inflammatory reaction which damages the respiratory epithelium and thus, increases susceptibility to infection while also causing fibrosis and narrowing of the airways in the long term. With time cardiovascular

function worsens, as evident from the low oxygen saturation levels. The body compensates for the hypoxia by producing erythropoietin which also explains the elevated RBCs, haematocrit, and haemoglobin levels. Congestive Heart Failure Heart failure is the inability of the heart to pump enough blood to meet the metabolic demands of vital organs and tissues (Inamdar & Inamdar, 2016). The term congestion is applicable when blood pools in the systemic circulation, this is evident by the engorged neck veins in this patient (Bricker, 2021). Furthermore, because of the pooling of blood in the systemic circulation, the hydrostatic pressure increases resulting in pitting oedema in the dependent part of the body, which was also evident during the physical examination of this patient. Dyspnoea is another common finding in congestive heart failure due to the diminished oxygen supply to vital organs. Dyspnoea can also possibly account for secondary polycythaemia (Berliner et al., 2016). Moreover, male gender, advanced age, and cigarette smoking are known risk factors in the development of congestive heart failure (Chamberlain et al., 2020). The only parts of the patients' history that this diagnosis cannot explain are the frequent bouts of fever, chronic cough, and purulent sputum. For this reason, although congestive heart failure remains a plausible diagnosis, COPD remains as the most plausible is still the most likely.

Bronchiectasis Bronchiectasis is a chronic lung disease characterised by chronic productive cough and repeated lung infections (Bird & Memon, 2021). The repeated lung infections can damage airway epithelium, limiting the supply of oxygen to alveoli and therefore causing dyspnoea. Concurrently, haemoptysis is a frequent finding in bronchiectasis (Ittrich et al., 2017). However, bronchiectasis is also characterised by weight loss, unlike the weight gain in this case, and does not explain ...