NSG 528 Presentation PDF, February 2023

NSG 528 PRESENTATION SUBMITTED BY GROUP D/4 MEMBERS: FALEYE, OLURANTI VICTORIA: 206838 AKINDEHIN, AYOMIDE DEBORAH: 198632 KAMORUDEEN, SHUKROH ADERONKE: 206840 PINMILOYE, AYOMIDE MICHAEL: 206849 AKINGBADE, OLUWATOBI ADURAGBEMI: 206832 COURSE: PALLIATIVE CARE NURSING (NSG 528) LECTURER IN CHARGE: DR I...

NSG 528 PRESENTATION SUBMITTED BY GROUP D/4 MEMBERS: FALEYE, OLURANTI VICTORIA: 206838 AKINDEHIN, AYOMIDE DEBORAH: 198632 KAMORUDEEN, SHUKROH ADERONKE: 206840 PINMILOYE, AYOMIDE MICHAEL: 206849 AKINGBADE, OLUWATOBI ADURAGBEMI: 206832 COURSE: PALLIATIVE CARE NURSING (NSG 528) LECTURER IN CHARGE: DR IFEOLUWA KOLAWOLE IN PARTIAL FULFILLMENT OF THE AWARD OF BACHELOR OF NURSING SCIENCE DEGREE. FEBRUARY, 2023. 1 TABLE OF CONTENT The Repiratory Problems (Dypsnea) Introducton 4 Causes 4 Signs and symptoms 4 Management 5-9 Respiratory Secretions 9 Causes 9-10 Treatment 11-12 Malignant Plural Effusion (MPE) Introduction 13 Pathophysiology of MPE 13-14 Causes 14 Signs and symptoms 15 Management 15 Conclusion 16 Airway Secretion Infection Introduction 17 Causes 17-18 Signs and symptoms 18 Prevention 18 Management 19-20 2 Hemoptysis Introduction 22 Causes 22-23 Signs and Symptoms 23 Management 23-26 Epistaxis Introduction 26 Causes 26 Management 27-28 References 29-31 3 THE RESPIRATORY SYSTEM The respiratory system is composed of the upper and lower respiratory tracts The two tracts are responsible for ventilation. The upper respiratory tract warms and filters inspired air so that the lower respiratory tract can accomplish gas exchange. Gas exchange involves delivery oxygen to the tissues through the bloodstream and expelling waste gases during expiration ANATOMY Upper respiratory tract It includes the nose, sinuses, nasal passages, pharynx, tonsils, adenoids, larynx, and trachea. NOSE. It is the passageway for air to pass to and from the lungs. It filters impurities and humidifies and warms air as it is inhaled. The nose has both external and internal portions. The external protudes from the face are supported by the nasal bones and cartilage. The anterior nares are the external openings of the nasal cavities. The internal portion of the nose is a hollow cavity separated into the right and left nasal cavities known as the septum. 4 As air enters into the nostril, it deflects upwards to the throat through nose and follows a circuitous route before it reaches the nasopharynx. It comes into contact with a large surface of moisture, warm, and highly vascularized ciliated mucous membranes that traps practically all dust and microorganisms in the inhaled hair. PARANASAL SINUSES It includes 4 pairs of bony cavities that are lined with nasal mucosa and ciliated pseudostratified columnar epithelium. The sinuses are named by their location. The frontal, ethmoidal, spherical, and maxillary. The function of the sinuses is to serve as a resonating chamber in speech, and it's a common site of infection. PHARYNX, TONSILS AND ADENOIDS The pharynx is a tube like structure that connects the nasal and oral cavities to the larynx. The nasopharynx is located posterior to the nose and above the soft palate. The oropharynx house is the facial or palatine, tonsils. The laryngopharynx extends from the hyoid bone to the cricoid cartilage. The eppiglotis forms the entrance for the larynx. The adenoids are located at the roof of the nasopharynx. The tonsils and adenoids encircle the throat. These structures are important links in the chain of lymphnodes guarding the throat. The pharynx acts as a passageway for the respiratory and digestive tracts. LARYNX It's a cartilaginous epithelium lined structure that connects the pharynx and the trachea. The major function is vocalisation. It protects the lower airway from foreign substances and facilities coughing. It consists of the epiglottis, grottos, thyroid cartilage, cricoid cartilage, arytenoid cartilage, and vocal cords. TRACHEA 5 It's composed of a C shaped ring of cartilage. It's serves as a passage between the larynx and bronchi. Lower Respiratory Tract. It's composed of lungs (bronchial and alveolar structures needed for gas exchange). LUNGS They are paired elastic structures, which are airtight chamber with distensible walls. The lungs are the primary organs of the lower respiratory tract and are housed within the thoracic cavity.They are divided into lobes , with the right lung having three lobes and the left lung having two lobes to accommodate the heart. They are surrounded by a double-layered membrane called the Pleura which helps to reduce friction during breathing movements. MEDIASTINUM The mediastinum is a central compartment of the thoracic cavity located between the lungs. It is bordered by the sternum in front, the vertebral column at the back, and the lungs on each side BRONCHI AND BRONCHIOLES The trachea branches into two primary bronchi, one entering each lung. Each primary bronchus then subdivides into secondary and tertiary bronchi, further branching into smaller bronchioles. Bronchi are lined with ciliated epithelial cells and mucus-producing goblet cells, which help to trap and remove debris and pathogens from the air. BRONCHIOLES Bronchioles are smaller branches of the bronchi that lack cartilage in their walls. They continue to branch into even smaller bronchioles, eventually leading to the alveoli. Smooth muscle surrounds bronchioles, allowing them to regulate airflow by constricting or dilating in response to signals from the nervous system. 6 ALVEOLI Alveoli are tiny, grape-like air sacs at the end of the bronchioles where gas exchange occurs. They are surrounded by a network of capillaries, allowing for the exchange of oxygen and carbon dioxide between the air in the alveoli and the blood in the capillaries. The walls of the alveoli are extremely thin to facilitate efficient gas exchange. Surfactant, a substance produced by alveolar cells, help to reduce surface tension within the alveoli, preventing their collapse during exhalation. Functions of the respiratory system Gas Exchange: The primary function of the respiratory system is to facilitate the exchange of oxygen (O2) and carbon dioxide (CO2) between the body and the external environment. During inhalation (inspiration), oxygen-rich air enters the lungs and diffuses into the bloodstream through the alveoli, where it binds to hemoglobin in red blood cells for transport to tissues. Simultaneously, carbon dioxide, a waste product of cellular metabolism, diffuses from the bloodstream into the alveoli to be exhaled during exhalation (expiration). Oxygen Transport: Oxygen is essential for cellular respiration, the process by which cells produce energy in the form of adenosine triphosphate (ATP) through the breakdown of glucose. The respiratory system ensures that an adequate supply of oxygen is delivered to tissues and organs throughout the body to sustain cellular functions and metabolism. Carbon Dioxide Removal: Carbon dioxide is a waste product of cellular metabolism that must be eliminated from the body to maintain proper acid-base balance and prevent acidosis. The respiratory system removes carbon dioxide from the bloodstream by exchanging it for oxygen in the alveoli, which is then exhaled from the body during expiration. pH Regulation: 7 The respiratory system plays a crucial role in regulating the pH of the blood by controlling the levels of carbon dioxide. Carbon dioxide reacts with water in the blood to form carbonic acid, which can lower blood pH if levels become too high (acidosis). By adjusting respiratory rate and depth, the body can increase or decrease the elimination of carbon dioxide to maintain optimal blood pH. Protection against Pathogens and Irritants: The respiratory system includes mechanisms to protect the lungs from harmful pathogens, irritants, and pollutants present in the air. Mucus-producing cells in the respiratory tract trap foreign particles and microorganisms, while cilia lining the airways sweep them toward the throat to be expelled or swallowed. Additionally, specialized immune cells in the lungs, such as macrophages, help to engulf and destroy pathogens to prevent respiratory infections. Regulation of Blood Pressure: Respiratory functions, particularly breathing rate and depth, can influence blood pressure through their effects on arterial blood gases and vascular resistance. Changes in respiratory patterns can lead to alterations in blood pressure, which is important for maintaining cardiovascular homeostasis and perfusion to vital organs RESPIRATORY PROBLEMS IN PALLIATIVE CARE DYSPNOEA Dyspnoea is the distressing awareness of the process of breathing - either the frequency or the effort involved. It is very frightening and is one of the most common symptoms in palliative care. It is extremely common with advancing disease, particularly late stages of chronic obstructive pulmonary disease (COPD), chronic heart failure, asthma cancer, and neurological or muscular disease, and is also common in end-stage kidney disease and acquired immune deficiency syndrome (AIDS). Dyspnoea is common in people with cancer in general, but it is more common and severe in people with primary lung cancers (affecting 90% of those with advanced lung cancer). 8 It involves perception of breathlessness and a person's reaction to it, and anxiety may contribute significantly. There is no universally accepted measure of breathlessness in palliative care patients and several scales are in use, most looking at the functional impact of the breathlessness. Self-rating scales may be helpful in assessment and monitoring of response to treatment. CAUSES OF DYSPNOEA Dyspnoea can be caused by either reversible or irreversible mood changes. Causes of dyspnoea Infection Bronchoconstriction Pleural or pericardial effusion Potentially reversible or partially reversible with further treatment Pneumothorax Pulmonary embolism Cardiac failure/dysrhythmia/anaemia Panic or psychological disorder Superior vena cava obstruction Lymphangitis Ascites Progression of disease (eg, malignant infiltration, fibrosis, congestion) leading Irreversible to diminished lung function Progression of neurological or muscular disease preventing adequate ventilation SIGNS AND SYMPTOMS Difficulty catching breath. Noisy breathing. 9 Very fast, shallow breaths. Tachycardia. Wheezing Chest pain. Cyanosis. Cold, clammy skin. Anxiety or panicky feelings. Coughing Feeling of suffocation. Heart palpitations. MANAGEMENT OF DYSPNOEA Management should start with optimising the treatment of any underlying causes of breathlessness, especially bronchoconstriction. Non-pharmacological treatments should then be considered, in particular, positioning and breathing techniques, mobility aids, and muscle strengthening. Simple aids, such as a hand-held fan, are also important. Anxiety inevitably accompanies the symptom and can be alleviated by explaining the current situation and management options. Explore ongoing fears (fears of suffocation, choking, dying in sleep are common). Useful strategies include: 10 o Positioning - the most comfortable position is usually sitting upright with support. o Keeping the room cool. o Moving air from a fan (hand-held or stationary) or open window helps provide psychological relief. o Teaching and use of breathing exercises and relaxation methods. Breathing retraining, taught by physiotherapists or clinical nurse specialists. o Encourage modification of lifestyle in reducing non-essential activities, while trying to maintain mobility and independence as far as possible. o Encourage exertion to the point of breathlessness to build tolerance and maintain fitness - this will vary considerably between individuals. Pulmonary rehabilitation appears to be well-tolerated and to provide symptomatic relief in many patients with severe COPD. It is increasingly being used in a palliative setting. o Dietary modifications with small frequent drinks and meals being best tolerated. Patients with cancer or end-stage respiratory disease are frequently cachectic and advice from a dietician may be helpful. o Mouth breathing dries the mouth and oxygen will be very dry unless it has been humidified, so attention to oral hygiene is important. o Complementary therapies such as aromatherapy, hypnosis and acupuncture may be helpful to some patients but the evidence base is weak. 11 MEDICAL INTERVENTIONS Physical interventions may help to relieve or even reverse the cause of the dyspnoea. Discussing possible eventualities can help patients make important, informed decisions about their future care such as the need for emergency hospital admissions, use of artificial ventilation and aggressive treatment of infections. PRIMARY CARE Treatment of reversible or partially reversible causes of dyspnoea. For example: Optimising treatment of asthma, COPD, heart failure. Infections will aggravate dyspnoea and treatment of the infection will improve matters where the patient is not strictly terminal. SECONDARY CARE Blood transfusion - anaemia can exacerbate dyspnoea on exertion, and blood transfusion can be justified on this basis. One study looking at practice in six British hospices found that patients received blood transfusions in about 6% of all hospice admissions. Treatment of the underlying disease - for example: o Pleural effusion tapping- for recurrent effusion, pleurodesis is often effective, but it is a painful procedure. o Tapping ascites can relieve pressure on the diaphragm and improve ventilation. o Superior Vena Cava(SVC) obstruction can arise from compression of the SVC by mediastinal tumour. In three quarters of cases it is from primary lung tumours but intraluminal thrombosis may also occur. There is dyspnoea and gross venous congestion and oedema of the head, neck and upper limbs. High-dose steroids with radiotherapy or chemotherapy may help. Dilatation, stenting and anticoagulants may also be tried. o Tumour may impinge on the trachea or bronchus, causing collapse of a segment or of a complete lung. Treatments include steroids, external 12 radiotherapy, chemotherapy (for small-cell cancer of the lung) and endobronchial treatments such as laser, radiotherapy, stenting, cryotherapy and balloon dilatation. Emergencies such as pulmonary embolism and pneumothorax may justify admission to hospital for active treatment. DRUGS OPIATES Reticence about the use of morphine for palliation of dyspnoea is common, especially in nonmalignant disease (COPD in particular), for fear of causing respiratory depression. Oral and parenteral opiates are widely accepted as providing good symptom relief, and the risk of significant respiratory depression appears to be negligible. Oral morphine is widely used to manage dyspnoea. The anxiolytic and antitussive effects of diamorphine make it ideal for lung cancer. Oral morphine can be used safely for the management of dyspnoea, even with COPD, if the patient is started on a low dose, and it is titrated according to response and sideeffects. Patients not already receiving morphine should start at doses of 5 mg 4hourly/prn. For those already on morphine, whether for pain or dyspnoea, the overall dose may need to be increased by 30% to 50%. When the oral route is no longer available, administration by continuous subcutaneous infusion is acceptable. It may be combined with a benzodiazepine. The use of nebulised opiates is not recommended. In extreme dyspnoea and distress, intravenous or subcutaneous diamorphine is often used for more rapid relief than by the oral route. ANXIOLYTICS There is as much reason to be cautious about respiratory depression with benzodiazepines as with opiates but they are commonly used to treat dyspnoea in palliative care. There is no evidence for a beneficial effect of benzodiazepines for the relief of dyspnoea associated with cancer or COPD. However, guidelines continue to recommend their use for reducing anxiety 13 associated with breathlessness, as they reduce the hypoxic or hypercapnic ventilatory responses, and the emotional response to dyspnoea. Diazepam, lorazepam and midazolam are most frequently used. Selection is dependent on the stage of terminal disease, the severity of anxiety, and the desired onset of action. Lorazepam can be given sublingually (0.5 mg 4-6 hourly); midazolam is usually used subcutaneously (5-20 mg over 24 hours). Tricyclic antidepressants and selective serotonin reuptake inhibitors (SSRIs) may be helpful, especially for panic attacks. OXYGEN THERAPY The role of oxygen therapy for palliation of dyspnoea is unclear, and there is as yet no convincing evidence of benefit. Currently recommendations suggest oxygen should be used only where the patient is shown to be hypoxic. A person's need for oxygen therapy should be clinically assessed including potential risks from the oxygen use (for example, a smoker in the household). Short-burst oxygen therapy should be initiated at 2 L/minute for an initial duration of treatment of between 15 and 30 minutes (although others suggest continuing until benefit is felt). Either a mask or nasal cannulae may suit patient preference and comfort. RESPIRATORY SECRETIONS First-line treatment is hyoscine butylbromide 20 mg subcutaneously hourly as required in the final stages of life. Glycopyrronium bromide 200 micrograms 6- to 8-hourly as required and hyoscine hydrobromide 400 micrograms 2-hourly are other options. COUGH Cough in people with people with cancer is most commonly associated with cancer of the airways, lungs, pleura, and mediastinum, but tumours metastasizing to the thorax can also cause cough. In people with cancer, the most common cause of acute cough is respiratory tract 14 infection. The most severe cough is convulsive, unending, and permits no other object of attention. COMMON GENERAL CAUSES Cough in palliative care patients can be due to causes similar to those in the general population. In some patients, the cough is an indication that there is an exacerbation of a comorbid illness (such as COPD or bronchiectasis) or an acute pulmonary infection that can be treated. Cough may also be due to conditions which can be relatively easily addressed, such as gastroesophageal reflux disease (GERD), or caused by a medication side effect (eg, angiotensin-converting enzyme [ACE] inhibitors). While cessation of cigarette smoking (or other inhaled irritants) is useful as a response to resultant cough in the general population, smoking cessation is often not realistic and/or helpful in patients with a limited prognosis of weeks or a short number of months. SPECIFIC CAUSES IN PALLIATIVE CARE — Certain causes of cough are more common in palliative care patients. Ineffective swallowing — In palliative care populations, the cough reflex is often stimulated by attempts to clear accumulating secretions due to asthenia, muscle weakness, and the inability to coordinate an effective swallow. Typical patient signs may include drooling and cough brought on by eating and/or drinking. Malignant disease — Malignancies likely to cause cough include those of the airways, lungs, pleura, and mediastinum, or cancers that metastasize to the thorax. Cough is present in up to 90 percent of patients with advanced lung or head and neck cancer. Chronic infections — In palliative care patients with cystic fibrosis or other chronic lung disease, chronic infections may contribute to cough symptoms. In such cases, antibiotics may be useful for palliative suppression of cough. 15 TREATMENT Palliative treatment options for endobronchial tumors include chemotherapy, radiotherapy, endobronchial laser resection, or stent placement. As a general rule, cough improves if directed therapy reduces the impact of the cancer. However, symptom improvement with palliative chemotherapy, radiotherapy, or endobronchial brachytherapy may take several weeks. Symptom-directed treatment — The mainstay of symptom-directed pharmacologic therapy is cough suppression with antitussives, which can be used alone or alongside disease-specific treatments. MILD COUGH Mild cough — For patients with mild cough, nonpharmacologic therapies can be used as a first step. Options include use of a linctus such as honey, breathing exercises, cough suppression techniques, and patient counselling If these are ineffective, peripherally acting antitussive (eg, benzonatate) can then be used. Benzonatate presumably anesthetizes stretch receptors in the lungs and pleura. The recommended dose is 100 to 200 mg three times daily. Moderate to severe cough — Centrally active agents are appropriate for patients with moderate to severe cough, including cough that impairs sleep and cough that does not respond to peripherally acting agents. Opioids can be used as first-line treatment, or, if opioids are contraindicated, gabapentin or pregabalin. Nebulized local anesthetics, such as lidocaine or bupivacaine are most likely to be used in specialized palliative care units. OPIOIDS — Opioids are a mainstay of pharmacologic therapy for palliative care patients with moderate to severe chronic cough, particularly those with intrathoracic cancer. Appropriate options for cough suppression in opioid-naïve patients include: Morphine 5 mg by mouth every four hours as needed for moderate to severe cough. If benefits from routine use of immediate release opioids are demonstrated, long-acting preparations can be considered for constant cough. Similar equianalgesic dosing of 1 to 2 mg intravenously (IV) or 16 subcutaneously can be utilized if the patient is unable to take oral medications or for ease of administration especially in the hospital setting. A different opioid at equianalgesic dosing to morphine 5 mg by mouth also can be utilized. For patients already receiving opioids for pain, a 25 to 50 percent dose increase may be tried to suppress the cough. Codeine 15 mg orally every four hours as needed is an appropriate dose for cough suppression. However, codeine is metabolized to morphine by a cytochrome P450 enzyme, and patients who have variants of this enzyme, are at risk of experiencing adverse effects of codeine without the benefit. GABAPENTIN AND PREGABALIN — Alternative or concurrent treatments for chronic cough are the gamma aminobutyric acid (GABA) analogs gabapentin and pregabalin. These agents can be used for patients with moderate to severe cough who are unable to take opioids. Gabapentin is initiated at a low dose (300 mg/day) with gradual increases until cough relief, dose-limiting adverse effects, or a dose of 900 mg twice daily is achieved. Patients should be monitored for sedation, which typically wanes one to three days after each dose escalation. Additional adverse effects may include dizziness, diarrhea, nausea, emotional lability, somnolence, nystagmus, tremor, weakness, and peripheral edema. Pregabalin is initiated at a low dose (eg, 75 mg/day) and gradually increased over a week to 300 mg/day to minimize sedation and dizziness. While gabapentin may help with treatment of chronic cough, it may also have a more specific role in treating refractory gastroesophageal reflux-induced cough. RARE USE OF COMBINATION THERAPY — Concomitant use of opioids and GABA analogs can be attempted if there is concern that a component of the cough may be due to nerve irritation and thus not completely managed with opioids alone. However, this combination of agents must be approached with caution due to the possibility of significant adverse side effects of increased sedation and risk of opioid-related death. 17 INTRODUCTION TO MALIGNANT PLURAL EFFUSION Malignant pleural effusion (MPE) is a serious condition characterized by the accumulation of fluid in the pleural cavity, the space between the lungs and the chest wall, resulting from the spread of cancer to the pleura. This condition poses significant challenges in terms of diagnosis and management, requiring a multidisciplinary approach. Definition: Malignant pleural effusion occurs when cancer cells invade the pleura, leading to an inflammatory response and the accumulation of fluid in the pleural space. It is often associated with advancedstage cancer and can originate from various primary malignancies, including lung cancer, breast cancer, and malignant mesothelioma. Pathophysiology of Malignant Pleural Effusion The pathophysiology of malignant pleural effusions (MPE) involves a complex interplay of factors related to both the cancer cells and the pleural space. The following are the pathophysiological process involved in MPE: Cancer Cell Invasion: Malignant pleural effusions typically occur when cancer cells invade the pleura, which is the thin membrane covering the lungs and lining the chest cavity. Cancer cells can spread to the pleura through direct extension from nearby tumors or via hematogenous and lymphatic routes. Inflammatory Response: The invasion of cancer cells triggers an inflammatory response in the pleura. This inflammation disrupts the normal balance between fluid production and absorption in the pleural space. Increased Vascular Permeability: Cancer-related inflammation leads to increased vascular permeability in the pleura. This allows fluid, proteins, and cancer cells to leak into the pleural space. 18 Production of Pleural Fluid: The pleura normally produces a small amount of fluid that lubricates the space between the lung and chest wall, facilitating smooth movement during breathing. However, in MPE, the cancerinduced inflammatory changes disrupt this balance, leading to excessive fluid production. Impaired Fluid Drainage: Cancer cells and the inflammatory environment can impair the normal drainage of fluid from the pleural space. This results in the accumulation of fluid, causing pleural effusion. Mechanical Effects: As pleural effusion accumulates, it exerts pressure on the lung, causing compression and collapse. This compression contributes to symptoms such as dyspnea and chest pain. Cytokine and Growth Factor Release: Cancer cells release various cytokines and growth factors that further contribute to inflammation and fluid accumulation. These molecular signals play a role in promoting tumor growth and survival in the pleura. Angiogenesis: MPE is associated with angiogenesis, the formation of new blood vessels, in the pleura. This process is driven by factors released by cancer cells and promotes the blood supply necessary for tumor growth. Causes of MPE The primary cause of malignant pleural effusion is the infiltration of cancer cells into the pleura. This infiltration disrupts the normal balance between fluid production and absorption in the pleural space, resulting in fluid accumulation. Common primary cancers associated with MPE include lung and breast cancers, but it can also occur in other malignancies. 19 Signs and Symptoms MPE Patients with malignant pleural effusion may experience symptoms such as Dyspnea (shortness of breath), cough, chest pain, and weight loss. Physical examination may reveal decreased breath sounds on the affected side, and imaging studies like chest X-rays or CT scans can confirm the presence of pleural effusion. Management: The management of malignant pleural effusion aims to relieve symptoms, improve quality of life, and address the underlying cancer. Treatment options include: Thoracentesis :Thoracentesis involves draining the accumulated fluid from the pleural space to alleviate symptoms temporarily. Pleurodesis: is a procedure that induces adhesion between the two layers of the pleura, preventing further fluid accumulation. Chemotherapy and Radiation Therapy:Targeted chemotherapy specific to the underlying cancer is often employed to control cancer growth and reduce pleural effusion. Radiation therapy :may be used to target the malignant cells in the pleura. Intrapleural Catheters:Intrapleural catheters can be placed to drain and manage recurrent pleural effusion, providing a more long-term solution. Systemic Cancer Treatment:Treating the primary cancer with systemic therapies, such as immunotherapy or targeted therapy, may help control the spread of cancer and alleviate pleural effusion. Supportive Care:Palliative care is essential for symptom management and improving the patient's overall quality of life. 20 Conclusion It's crucial for patients with malignant pleural effusion to receive personalized care, and treatment decisions should be made in consultation with a multidisciplinary team of oncologists, pulmonologists, and other specialists. Regular follow-up and ongoing supportive care are essential components of managing this challenging condition. 21 AIRWAY SECRETIONS INFECTION The airway secretions, also known as respiratory mucus, are identified in all vertebrates, where they form a continuous lining filter on the epithelium surface. This mechanical and biochemical barrier protects the epithelial cells from invasion and injury by microorganisms and noxious agents present in the environment. Infections of the airway secretions can occur when pathogens such as bacteria, viruses, or fungi invade the respiratory tract. These infections can lead to symptoms such as coughing, wheezing, difficulty breathing, fever, and production of discolored or foul-smelling mucus. Common examples include bronchitis, pneumonia, and sinusitis. Treatment typically involves antibiotics, antiviral medications, or antifungal drugs, depending on the underlying cause of the infection. It's important to seek medical attention if you suspect an infection in your airway secretions, especially if symptoms are severe or persistent. CAUSES Excessive respiratory secretions can be classified as: Type I: caused by salivary secretions Type II: caused by the build-up of fluid in the lungs. It's often the result of pulmonary disease, e.g. COPD, asthma, bronchitis, bronchiectasis, cystic fibrosis and lung cancer. Other forms of causes include: The causes of airway secretion infections can vary but commonly include: 1. Viruses: Respiratory viruses such as influenza, rhinovirus, respiratory syncytial virus (RSV), and adenovirus can infect the airway secretions, leading to conditions like the common cold, influenza, and viral bronchitis. 22 2. Bacteria: Bacterial infections such as Streptococcus pneumoniae, Haemophilus influenzae, and Mycoplasma pneumoniae can cause bacterial bronchitis, pneumonia, and other respiratory tract infections. 3. Fungi: Fungal infections such as Aspergillus and Candida can infect the airways, particularly in individuals with weakened immune systems or underlying lung conditions. 4. Environmental Irritants: Exposure to pollutants, cigarette smoke, or other environmental irritants can damage the respiratory tract's lining, making it more susceptible to infection. 5. Allergens: Allergens such as pollen, dust mites, and pet dander can trigger allergic reactions in the airways, leading to conditions like allergic rhinitis or asthma, which may predispose individuals to respiratory infections. 6. Immunocompromised State: Conditions or medications that weaken the immune system, such as HIV/AIDS, chemotherapy, or immunosuppressive drugs, can increase the risk of airway secretion infections. 7. Anatomical Abnormalities: Structural abnormalities in the respiratory tract, such as nasal polyps or deviated septum, can impair mucociliary clearance and predispose individuals to infections. 8. Underlying Medical Conditions: Chronic conditions like chronic obstructive pulmonary disease (COPD), cystic fibrosis, or bronchiectasis can alter the normal function of the airways, making them more susceptible to infections. 23 SIGNS AND SYMPTOMS Continuous cough High temperature, fever or chills Loss of or change in, your normal sense of taste or smell Shortness of breath Unexplained tiredness, lack of energy Muscle aches or pains that are not due to exercise Not wanting to eat or not feeling hungry Headache that is unusual or longer lasting than usual Sore throat, stuffy or runny nose Diarrhoea Feeling sick or being sick PREVENTION Good hand hygiene Avoiding close contact with sick individuals, Staying up-to-date with vaccinations (e.g., influenza and pneumonia vaccines) Minimizing exposure to environmental pollutants TREATMENT/MANAGEMENT PHARMACOLOGICAL MANAGEMENT Antibiotics, Antiviral and Antifungal (e.g Amoxicillin, Azithromycin, fluconazone, Caspofungin, Ribavirin) Antipyretic (Aspirin, Acetaminophen) Cough suppressant/Expectorant (Dextromethorphan, Pholcodine) 24 MEDICAL MANAGEMENT Vaccination Saline nasal irrigation Humidification Rest Regular fluid intake 25 HAEMOPTYSIS Haemoptysis is expectoration of blood originating from the lower respiratory tract rather than from an upper airway or gastrointestinal source, with clinical manifestations varying from small amounts of blood-streaked sputum to life-threatening haemorrhage (massive haemoptysis) that requires immediate management due to risk of asphyxia, cardiovascular collapse, and death (Radchenko et al., 2019). Haemoptysis may be idiopathic or may indicate underlying condition such as bronchiectasis, fungal infection, lower respiratory tract infection, lung cancer, or tuberculosis, it is also called pulmonary haemorrhage, Pulmonary bleeding, Airway haemorrhage, Coughing up blood (Larici et al., 2023). Haemoptysis must be differentiated from pseudohemoptysis (expectoration of blood originating in the nasopharynx or oropharynx) and hematemesis (vomiting of blood). Pseudohemoptysis can be diagnosed by inspection of the nasopharynx and oropharynx, and hematemesis by other gastrointestinal symptoms and risk factors for gastrointestinal tract bleeding. Characteristics of the expectorated material that suggest that a gastrointestinal source is unlikely include an alkaline pH, foaminess, and/or the presence of pus. Life-threatening haemoptysis is generally used to describe the expectoration of a large amount of blood and/or a rapid rate of bleeding, although the precise thresholds that constitute life-threatening haemoptysis are controversial. Some define life-threatening haemoptysis as ≥150 mL of expectorated blood over a 24-hour period or bleeding at a rate ≥100 mL/hour. PATHOGENESIS AND UNDERLYING CAUSES In palliative care populations, haemoptysis often arises from high-pressure bronchial circulation but can occur in patients via erosion of tumour or when low-pressure pulmonary capillaries are affected by inflammation. This can occur with primary or secondary lung cancer, terminal haematological malignancy, lung infection or abscess, bronchiectasis, pulmonary embolism, cystic fibrosis (Stenekes et al. 2023), bleeding disorders, anticoagulant use, anti-GBM (Goodpasture) disease, granulomatosis with polyangiitis, and other less common conditions summarised in table 1 below. Pulmonary haemorrhage is also a known complication of the antiangiogenic agent bevacizumab, especially in patients with squamous cell bronchogenic carcinoma. The use of bevacizumab is contraindicated in patients with squamous cell lung carcinoma and in any patient with haemoptysis (>2.5 mL of blood) within three months. 26 Possible causes Examples Hematologic Coagulopathy, Disseminated intravascular coagulation, Thrombocytopenia, platelet dysfunction Pulmonary Bronchiectasis, Cystic fibrosis, Bullous emphysema, Pulmonary embolism Infection Fungal infection, Necrotizing Pneumonia, Lung Abscess, Parasitic Infection, Septic pulmonary embolism, Tuberculosis, Viral Infection Iatrogenic from diagnostic Bronchoscopy, Pulmonary artery rupture, or therapeutic procedure Transtracheal aspiration Neoplastic Bronchogenic carcinoma, Metastatic Cancer Drugs or Toxins Anticoagulants, Aspirin, Thrombocytopenia agents Systemic diseases Anti GBM (Good pasture) syndrome, granulomatosis with polyangiitis, Systemic lupus erythematosus, Vasculitis Table 1: Causes of haemoptysis in palliative care CLINICAL MANIFESTATIONS Tachycardia Tachypnea Fever Low oxygen saturation rate Cachexia Patient distress (accessory muscle use, pursed lip breathing, agitation, decreased level of consciousness) Presence of crackles, rhonchi, strider, wheezing 27 MANAGEMENT Treatment should be tailored to the patient’s overall status, the severity of haemoptysis, the underlying cause, and the wishes of the patient and family or other loved ones. The patient and family/loved ones can often be best supported by the provision of goal-directed information and recommendations for management. It may be necessary to share prognostic information quickly to help determine the best goals of care and, subsequently, the best medical decisions. Using a team approach, psychosocial and spiritual needs can be addressed just as quickly as the physical symptoms. Minimizing patient and family distress – The palliative treatment of haemoptysis is primarily related to managing the experience of the patient, family, and other loved ones, as well as efforts to stop the bleeding if this is consistent with the overall goals of care. At a minimum, reassurance when the amount of blood is small is all that is required. Dark towels, dark sheets, dark blankets, and absorptive dressings with an impermeable backing can be used to diminish the visual impact. The environment can be managed by assuring that blood-tinged sputum is not collecting in a visible white cup at the bedside and that brilliant red-streaked blood on white tissues is kept from view. Life-threatening haemoptysis – Patients with life-threatening haemoptysis should be immediately placed into a position in which the presumed bleeding lung is in the dependent position (e.g., a patient whose right lung is bleeding should be placed in the right-side down decubitus position). The purpose of these positions is to protect the nonbleeding lung, since spillage of blood into the nonbleeding lung may prevent gas exchange by blocking the airway with clot or filling the alveoli with blood. Urgent palliative sedation – If haemoptysis is overwhelming and/or accompanied by severe hemodynamic instability and the goals of care do not support attempts at diagnosis or intervention, urgent sedation may be required. When urgent sedation is required, midazolam at 0.2 mg/kg administered intravenously (IV; if there is vascular access) or subcutaneously will be effective in the patient who is not chronically taking benzodiazepines. This is generally administered in 5 mg increments every five minutes until sedation is achieved. A continuous infusion may be instituted to maintain sedation. For the patient who is tolerant to benzodiazepines, an alternative agent, such as a barbiturate, will be effective, for example, 28 phenobarbital may be administered in a loading dose of 10 mg/kg intramuscularly (IM). Because of the relatively low concentration (it is available in 130 mg/mL vials), splitting of the total dose into two or three syringes with administration into separate IM sites may be required because of volume constraints. If phenobarbital is administered IV, the rate should not exceed 50 mg/minute. After sedation is achieved, a continuous infusion of 10 to 25 mg/hour can be instituted. A total dose of 600 to 2400 mg/day (25 to 100 mg/hour) is often sufficient to sustain sedation (Stirling et al., 2019). Temporizing measures – In the rare instances where the underlying cause can be reversed, diagnostic tests (bronchoscopy and, if an endobronchial lesion is not identified, angiogram to identify a feeder vessel that might be amenable to bronchial artery embolization (Fujita et al., 2023) and interventional procedures may be considered, if this is consistent with the goals of care. However, for patients with life-threatening haemoptysis, this might require urgent supportive care with blood or platelet transfusion, reversal of anticoagulation, and administration of procoagulant agents. Radiotherapy in a single dose may stop bleeding of a malignant source if the patient is stable enough for imaging and planning. Therapeutic bronchoscopy with balloon tamponade and infusion of vasoactive agents, such as epinephrine, may be successful as a temporizing measure. GUIDELINES FROM EXPERT GROUPS Guidelines are available for symptom management in patients with lung cancer from the American College of Chest Physicians (ACCP). For patients with haemoptysis, they recommend the following: For large-volume haemoptysis, the airway should be secured with a single-lumen endotracheal tube. Bronchoscopy is recommended to identify the source of bleeding, followed by endobronchial management options (e.g, argon plasma coagulation, laser endobronchial resection, or electrocautery for visible central airway lesions). For non-large-volume haemoptysis, bronchoscopy is recommended to identify the source of bleeding. For visible central airway lesions, endobronchial management options are recommended; for distal or parenchymal lesions, external beam radiotherapy is recommended. 29 If these measures are unsuccessful, consideration should be given to bronchial artery embolization to temporize the bleeding. EPISTAXIS Epistaxis is the medical term used to describe a nosebleed. Epistaxis is most often caused by trauma. In palliative care patients, epistaxis may be caused by a low platelet count or Weakened or damaged tissue/blood vessels due to radiation or a tumour (Traboulsi et al., 2019). CAUSES In palliative care, there is no specific cause and effect relationship with epistaxis (it could result from the disease condition or independent of it). it can be caused by variety of reasons like Trauma: Self-induced trauma from repeated nasal picking can cause anterior septal mucosal ulceration and bleeding. Nasal foreign bodies that cause local trauma (eg, nasogastric and nasotracheal tubes) can be responsible for rare cases of epistaxis. Dry weather: Low humidity may lead to mucosal irritation. Epistaxis is more prevalent in dry climates and during cold weather due to the dehumidification of the nasal mucosa by home heating systems. Drugs: Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs) are also frequently involved. Inflammation: Mucosal Inflammation due to the disease condition like rhinoscleroma can lead to epistaxis. Tumours: Benign and malignant tumours can manifest as epistaxis. Affected patients may also present with signs and symptoms of nasal obstruction and rhinosinusitis, often unilateral. Blood and vascular abnormalities: Low platelet count and weakened blood vessel can cause epistaxis. 30 MANAGEMENT OF EPISTAXIS In most patients with epistaxis, the bleeding responds to cauterization, nasal packing, or both. For those who have recurrent or severe bleeding for which medical therapy has failed, various surgical options are available. After surgery or embolization, patients should be closely observed for any complications or signs of rebleeding. Medical approaches to the treatment of epistaxis may include the following: Adequate pain control in patients with nasal packing, especially in those with posterior packing (However, the need of adequate pain control has to be balanced with the concern over hypoventilation in the patient with posterior pack.) Oral and topical antibiotics to prevent rhinosinusitis and possibly toxic shock syndrome Avoidance of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) Medications to control underlying medical problems (eg, hypertension, vitamin K deficiency) in consultation with other specialists First Aid Management Patients at increased risk of epistaxis are told to: Stay upright and lean slightly forward. Do not lie down or tilt head back. Apply firm pressure by pinching the bridge of the nose just below the bony ridge for at least five minutes. If the bleeding continues after five minutes, repeat the first two steps. It may help to apply ice to the bridge of your nose. After the bleeding has stopped, do not blow your nose as this may cause your nosebleed to start again. Use a cool-mist humidifier to keep the nasal mucosa moist and reduce the risk of nosebleeds. 31 HEALTH EDUCATION ON HOW TO PREVENT EPISTAXIS Patients are encouraged to: Use a saline nasal spray or saline nose drops two to three times a day in each nostril to keep your nasal passages moist. You can purchase these products over-the-counter or you can make them at home. To make the saline solution at home, mix 1 teaspoon of salt into 1 quart of tap water. Boil water for 20 minutes, and let cool until lukewarm. Avoid blowing your nose too forcefully. Sneeze through an open mouth. Always sneeze into a tissue or your elbow. Avoid putting anything solid into your nose, including your fingers. Quit smoking or not smoke Keep fingernails short 32 REFERENCES Cahil, B., Ingbar, D., (2019). Massive haemoptysis assessment and management. Clin chest med 15:147 Dezube, R. (2023). 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