Common lung diseases

Chest pain

There are several causes of chest pain ranging from a simple cutaneous irritation to the pain of a myocardial infarction. It is important for the physician to identify the source of the chest pain in order to adequately treat serious conditions. One of the common causes of chest pain related to the lungs is known as pleurisy. This is a sharp sensation associated with respiration or coughing. Patients with an infection or infarction of the lungs may complain of this sensation. Acute obstruction of the pulmonary veins by an embolus often presents with ischemic cardiac pain.

Chest pain associated with movement is more likely to be of musculoskeletal origin. Cardiac chest pain is a crushing sensation lasting more than 15 minutes and typically relieved with nitroglycerin. Some patients may also experience radiation of the pain up the left side of the neck and down the left upper limb.

Coughing

Coughing is actually a protective physiological mechanism designed to guard the airway. Receptors that facilitate this reflex are located in the mucosa of the caudal part of the upper respiratory tract (i.e. larynx, pharynx, and trachea) and bronchi. Exposure to irritants such as smoke, changes in the ambient temperature, drugs such as angiotensin-converting enzyme inhibitors, excessive mucus from a respiratory tract irritation, and aspiration of liquids or food particles are known triggers of the natural cough reflex. The aim of the reflex is to provide an expulsive mechanism to clear the airway and prevent obstruction.

Pathological coughing may occur as chronic persistent or acute transient symptoms of the underlying disease. Further classification of a cough refers to whether or not it is from a cardiovascular, respiratory, mechanical (i.e. foreign body obstruction), psychogenic (in panic disorders), or metabolic (lactic acidosis, salicylate poisoning, diabetic ketoacidosis) causes. A cough may be further characterized as a wet vs a dry cough. The former is usually associated with sputum production or suggests that there is a build-up of mucous within the airway; while the latter suggests that there is no associated hypersecretion.

Hemoptysis

Coughing up blood is likely to cause anyone to run to the nearest emergency room. However, this bleeding may originate from the gastrointestinal tract, cardiovascular system, or upper aerodigestive tract. Hemoptysis refers specifically to coughing up blood in the sputum; and is different from vomiting blood, which is hematemesis. The etiology of hemoptysis may be obscure at times and requires diligent investigation to identify the source of the bleeding. An encapsulated organism known as Streptococcus pneumoniae – which is the causative agent behind Pneumococcal pneumonia – may result in overt hemoptysis; but is also associated with a ‘rusty’- colored sputum. 

However, these symptoms are not unique to Pneumococcal pneumonia as patients with lung abscesses and other suppurative lung infections may also have these symptoms. Recurrent streaking of blood in sputum is usually suggestive of a bronchial malignancy or tuberculosis. A history of unintentional weight loss and nights sweats usually supports both etiologies and further investigation (plain film, computed tomography of the chest, sputum culture, or Mantoux testing) should be conducted. The most concerning underlying cause of hemoptysis is a pulmonary embolism, as this is acutely life-threatening.

Shortness of breath

Breathlessness is also referred to as being short of breath or dyspnea. It has a variety of benign and clinically urgent etiologies that can be identified with a thorough history and examination. Patients often describe it as an unsettling desire to breathe. This presentation may result from physical exercise in an unfit individual, but would rapidly resolve after a period of rest without leaving any deficits. Anxiety disorder is another cause of shortness of breath that can be identified with a thorough psychiatric history.

The healthcare professional should explore the patient history for the presence of chest pain, diaphoresis, nausea, or palpitations as these findings are suggestive of a cardiogenic source of dyspnea (i.e. decompensated heart failure or a myocardial infarction). An antecedent or concurrent history of stridor, wheezing, coughing, or hemoptysis is strongly indicative of a respiratory source of the dyspnea. Some patients with pre-existing conditions such as bronchial asthma, left heart failure, or chronic obstructive pulmonary disorders may have periodic episodes of breathlessness. The patient and caregivers should be educated regarding potential triggers that may cause them to decompensate and when to seek medical attention.

Summary of Common Presenting Complaints

Pneumonia

Pathogens must overcome a host of defense mechanisms in order to gain access to the lung parenchyma. The mucous secretions, cilia, lymphoid tissue, and resident macrophages all work synergistically to prevent microbes from settling in the lungs. Unfortunately, these mechanisms are not full-proof. Consequently, either viral, bacterial, fungal, or parasitic organisms can gain access to the parenchyma, leading to pneumonia. While the treatment of pneumonia depends on identification of the underlying pathogen, it is sometimes difficult to isolate the organism from the available specimen.

A crude way of determining the probable infectious organism is by determining when and where the patient fell ill. These pneumonia syndromes serve as a guide for clinicians to provide empirical treatment until culture studies are complete. These syndromes include:

• Community-acquired pneumonia (CAP) occurs in an otherwise healthy individual who was infected in the general environment. Bacterial agents commonly associated with community-acquired pneumonia include (but is not limited to) S. pneumoniae, H. influenzae, M.  catarrhalis, S. aureus, and K. pneumoniae. 
• Hospital-acquired pneumonia (HAP), otherwise called nosocomial pneumonia, occurs within 2 days of being admitted to the hospital. There is a predilection for elderly patients and those who have been receiving ventilator support (i.e. ventilator-associated pneumonia). A mixture of gram-positive (S. aureus, S. pneumonia) and gram-negative (E. coli, Pseudomonas species, K. pneumoniae) bacteria are commonly associated with this disorder. Patients with hospital-acquired pneumonia are also at risk of contracting antibiotic-resistant organisms such as methicillin-resistant Staphylococcus aureus (MRSA); which is associated with a higher mortality rate compared to pneumonia resulting from other microbes.
• Healthcare-associated pneumonia (HCAP) differs from hospital-acquired pneumonia in that these patients would have been admitted to the hospital for more than 2 days within the last 3 months. Alternatively, individuals who received hemodialysis, nursing facility residents, or recently received intravenous antibiotics or chemotherapy are also considered as healthcare-associated pneumonia patients. The offending organisms are similar to those found in hospital-acquired pneumonia.
• Aspiration pneumonia or aspiration pneumonitis results from the accidental passage of foreign substances into the airway. This phenomenon is often seen in patients who are unable to protect their airway from fluids being swallowed or regurgitated. Most commonly, gastric fluid is aspirated into the airway; resulting in the offending organisms being the anaerobes found in the gastric flora. 
• Pneumonia in the immunocompromised patient is caused by agents that would not normally result in an infection in a non-immunocompromised individual. These patients may have a defect in the defensive pathway of the respiratory tract either due to drug use (chemotherapy) or disease processes (e.g. leukemia, HIV). Viral (herpes virus, influenza virus), fungal (Pneumocystis jirovecii, Candida albicans), and bacterial (listed above) agents of varying degrees of virulence are able to cause an infection in some immunocompromised individuals.

Pneumonia can also be classified anatomically according to the pattern of infection observed on plain film radiographs. A lobar pneumonia is one in which an entire lobe of the lung (either unilateral or bilateral) is opaque. In contrast, lobular pneumonia refers to one in which only a segment of a lobe is affected. Interstitial pneumonia refers to diffuse opacification of the lung field in keeping with the disease of the supportive tissue of the lung (i.e. alveolar walls). This is also referred to as atypical pneumonia as the patient does not have the overt signs of pneumonia and the offending organism may be viral. Bronchopulmonary pneumonia is a condition in which the bronchioles and adjacent alveoli are infected. Consequently, the plain film shows patchy opacification throughout the lung fields. 

Tuberculosis

The incidence of tuberculosis has declined significantly due to the implementation of the Bacillus Calmette–Guérin (BCG) vaccine given between birth and 6 weeks of age. Unfortunately, it is still a significant contributor to the global mortality rate as it is the second most common cause of death resulting from an infectious agent. This potentially fatal bacterial pulmonary disease is caused by the Mycobacterium tuberculosis pathogen that can easily be passed from one individual to another through airborne respiratory droplets. Globally, the mycobacterial infection is more commonly observed among those of low socioeconomic status and among those living with HIV. This distribution also supports the pathogenesis of the infection as the microbes are spread through unpasteurized cow’s milk (M. bovis) or from person to person living in close contact with each other (M. tuberculosis).

The aerosolized mycobacterium them enters the alveoli, at which point the local macrophages are activated. The macrophages become Langhan’s and epithelioid cells that then form a granuloma around the affected area. This wall prevents further spread of the bacteria to unaffected lung tissue. As a result, tuberculosis can exist for years in a latent phase (latent tuberculosis). When multiple granulomas coalesce, they form a yellow, caseous nodule in the peripheral lung field known as a Ghon focus. If the mycobacterium spreads to the hilar lymph nodes then an identical pathological process ensues. Together, the main granuloma and the regional lymphadenopathy is called the primary complex of Ranke. The mycobacterium may spread hematogenously or via the lymphatic system, leading to extra-pulmonary disease that affects every organ system within the body.

Pulmonary embolism

The endothelial lining of the blood vessels is equipped with numerous mechanisms that inhibit the coagulation cascade within the vascular lumen. The German physician Rudolf Virchow described three factors that result in a prothrombotic state. Virchow’s triad speaks to the presence of venous stasis, endothelial injury, and a hypercoagulable state as predisposing factors that may result in the formation of a thrombus within the venous system. These thrombi often form in the deep venous systems and are subsequently referred to as deep vein thrombosis. While that is locally problematic, systemic complications arise when the thrombi embolize (i.e. venous thromboembolism) and migrate to the pulmonary arteries via the right heart. 

The resulting pulmonary embolism can present in three general patterns depending on the size of the embolus. In the acute setting, a small to medium sized pulmonary embolus may occlude a segmental artery; thus initiating the hypoxia, ischemia, infarction cascade. The patient may experience pleuritic-type chest pain that may limit respiration. The possibility exists that the patient may also experience hemoptysis. On examination, these patients are often tachycardic and mildly febrile, with stony-dull percussion in the presence of an effusion. A pleural rub and crackles may also be auscultated. Plain film radiographs may reveal a raised hemidiaphragm ipsilateral to the infarct and a pleural effusion. The only electrocardiographic change noted is sinus tachycardia and the arterial blood gas study may reveal reduced or normal values for the partial pressures of carbon dioxide and oxygen.

A massive pulmonary embolus in the acute setting is life-threatening. There is a significant reduction in the cardiac output and possibly acute right heart failure. Patients may complain of a central crushing chest pain, dyspnea, and syncope or collapse. Clinical findings in keeping with a massive pulmonary embolism include:

• Profound hypotension 
• Underlying tachycardia
• Elevated jugular venous pressure
• Loud P2
• Presence of an S3  gallop rhythm
• Reduced urine output
• Decreased blood oxygen saturation

There are usually no changes to the plain chest radiograph in the acute setting. However, the electrocardiograph may demonstrate a right bundle-branch block with inverted T-waves, deep S-waves in lead I, Q-waves and inverted T-waves in lead III, right axis deviation, peaked P-waves in lead II, and sinus tachycardia. Arterial blood gas studies show metabolic acidosis with significantly reduced partial pressures of carbon dioxide and oxygen. 

A small recurrent embolism occurring over time will have a cumulative destructive effect on the lungs and heart. This chronic pulmonary embolism obstructs the microvascular circulation of the lungs leading to increased pulmonary arterial pressure, right ventricular hypertrophy and subsequent dilatation, tricuspid regurgitation, right atrial hypertrophy and dilation, and subsequent right heart failure. Patients usually complain of shortness of breath on exertion and features of right heart failure (i.e. hepatomegaly, elevated JVP, decreased cardiac output, etc). Later on, in the disease process, the physician may detect a right parasternal heave, loud P2, and other features of right heart failure on clinical examination. A plain chest radiograph shows enlarged right ventricle and pulmonary trunk. This right ventricular enlargement along with the accompanying right heart strain can also be detected on electrocardiography. The arterial blood gas study may be normal at rest but if repeated following formal exercise, the partial pressure of oxygen will be reduced.

Pneumothorax

The thoracic cavity is a closed space under negative pressure that houses the lungs and mediastinum. Therefore, if there is an injury to the chest wall that allows communication with the external environment, then air will be pulled into the cavity. Additionally, spontaneous injury to the lung can also result in leakage and accumulation of air into the pleural space. In both cases, the resulting disorder is known as a pneumothorax. This disorder can occur spontaneously or secondary to a lung injury. Spontaneous primary pneumothorax tends to occur in tall individuals with a history of smoking and a predisposition to developing apical blebs (thin-walled air-filled sacs beneath the pleural membrane). The blebs may rupture with increased intrathoracic pressures such as Valsalva maneuvers or changes in atmospheric pressure (pilots and deep-sea divers). Iatrogenic, accidental, or malicious injury to the chest wall often results in a traumatic pneumothorax. These injuries may be associated with blood (hemopneumothorax), pus (empyema), or lymphatic fluid (chylothorax) within the pleural space. Additionally, the lung parenchyma may be compromised by an underlying infection or disease process that results in rupture of the lung parenchyma and leakage of air into the thorax. This is referred to as a secondary pneumothorax.

 If, after a rupture, the communication between the airway and thorax is sealed and the pleural pressure is still negative, then the leaked air may be reabsorbed. This is a simple or closed pneumothorax where the following reabsorption of air will cause the lungs to re-expand and no intervention is required. However, there are instances where there is continuous leakage of air into the chest cavity resulting in a mediastinal shift and subsequent kinking of the venae cavae. These cases are referred to as tension pneumothoraces and can be acutely life-threatening. This should be a clinical diagnosis with signs of:

• Use of accessory respiratory muscles
• Tracheal deviation away from the affected side
• Displaced apex beat away from the affected side
• Reduced tactile vocal fremitus on the affected side
• Hyper-resonant percussion note on the affected side
• Reduced vocal resonance on the affected side
• Reduced breath sounds on the affected side

There is not enough time for radiological investigations as the patient may expire on the way to the radiology suite. These patients require urgent needle decompression by introducing a 14 to 16 gauge (referring to the internal diameter of the needle) needle into the second intercostal space in the midclavicular line on the affected side. A sudden gush of air and restoration of the patient’s vital signs is indicative of adequate placement of the needle. This procedure should then be followed by placement of a thoracostomy tube in the 3rd to 4th intercostal space between the middle and anterior axillary lines under sterile conditions. The tube should then be connected to an underwater seal to prevent air from entering the chest cavity via this route. Placement of the tube can then be confirmed with a plain film chest radiograph.

Summary of disorders of the lungs

The table below contains a quick summary of the common pulmonary disorders and their subtypes.