Chest-Lower-Respiratory-Tract-Disorders.pdf

MANAGEMENT OF PATIENTS WITH CHEST AND LOWER RESPIRATORY TRACT DISORDERS part 1 Professor: Joseph Christian G. Bacleon, RN  TABLE OF CONTENTS INFLAMMATORY AND INFECTIOUS PULMONARY DISORDERS PART 1 ATELECTASIS PNEUMONIA ACUTE TRACHEOBRONCHITIS...

MANAGEMENT OF PATIENTS WITH CHEST AND LOWER RESPIRATORY TRACT DISORDERS part 1 Professor: Joseph Christian G. Bacleon, RN  TABLE OF CONTENTS INFLAMMATORY AND INFECTIOUS PULMONARY DISORDERS PART 1 ATELECTASIS PNEUMONIA ACUTE TRACHEOBRONCHITIS ASPIRATION LUNG ABSCESS INFLAMMATORY AND INFECTIOUS PULMONARY DISORDERS ATELECTASIS § Closure or collapse of alveoli § Acute or chronic § V/Q: ____________ ACUTE ATELECTASIS § most common § occurs in the postoperative setting ATELECTASIS § Closure or collapse of alveoli § Acute or chronic § V/Q: Low V/Q (Shunt) ACUTE ATELECTASIS § most common § occurs in the postoperative setting ATELECTASIS § Obstructive atelectasis is the most common type and results from reabsorption of gas (trapped alveolar air is absorbed into the bloodstream). § No additional air can enter into the alveoli because of the blockage. ATELECTASIS CAUSES: § Foreign body § Tumor or growth in an airway § Altered breathing patterns § secretions § Pain § Alterations in small airway function ATELECTASIS CAUSES: § Prolonged supine positioning § Increased abdominal pressure § Reduced lung volumes due to musculoskeletal or neurologic disorders § Restrictive defects § Specific surgical procedures ATELECTASIS PATHOPHYSIOLOGY: § Patients are at high risk for atelectasis postoperatively because of several factors. § A monotonous, low tidal breathing pattern may cause small airway closure and alveolar collapse. § Secretion retention, airway obstruction, and an impaired cough reflex may also occur. ATELECTASIS PATHOPHYSIOLOGY: § Bronchial obstruction – caused by secretions in patients with impaired cough mechanism, debilitated and bedridden. § Excessive pressure on the lungs tissue – restricts normal lung expansion on inspiration. ATELECTASIS PATHOPHYSIOLOGY: Pressure can be produced by: § Pleural effusion § Pneumothorax § Hemothorax ATELECTASIS CLINICAL MANIFESTATIONS: § Symptoms: insidious, increasing dyspnea, cough, and sputum production § Acute: tachycardia, tachypnea, pleural pain, and central cyanosis if large areas of the lung are affected § Chronic: similar to acute, pulmonary infection may be present ATELECTASIS ASSESSMENT & DIAGNOSTIC FINDINGS § Characterized by increased work of breathing and hypoxemia § Decreased breath sounds and crackles over the affected area § Chest x-ray may suggest a diagnosis of atelectasis before clinical symptoms appear § Pulse oximetry (SpO2) may demonstrate a low saturation of hemoglobin with oxygen (less than 90%) ATELECTASIS PREVENTION § Frequent turning § Early mobilization § Strategies to expand lungs and manage secretions § Incentive spirometer § Voluntary deep breathing § Secretion management § Pressurized metered-dose inhaler ATELECTASIS MANAGEMENT § Improve ventilation and remove secretions § First line measures: ü frequent turning, early ambulation, lung volume expansion maneuvers and coughing § Multidisciplinary: ICOUGH § PEEP, CPAP, bronchoscopy § CPT § Endotracheal intubation and mechanical ventilation § Thoracentesis to relieve compression ACUTE TRACHEOBRONCHITIS § an acute inflammation of the mucous membranes of the trachea and the bronchial tree. § Adequate treatment of upper respiratory tract infection is one of the major factors in the prevention of acute bronchitis ACUTE TRACHEOBRONCHITIS PATHOPHYSIOLOGY § The inflamed mucosa of the bronchi produces mucopurulent sputum. § A sputum culture is essential to identify the specific causative organism. § In addition to infection, inhalation of physical and chemical irritants, gases, or other air contaminants can also cause acute bronchial irritation. ACUTE TRACHEOBRONCHITIS CLINICAL MANIFESTATIONS INITIAL MANIFESTATIONS: § dry, irritating cough and expectorates a scanty amount of mucoid sputum. § sternal soreness from coughing and have fever or chills, night sweats, headache, and general malaise. ACUTE TRACHEOBRONCHITIS CLINICAL MANIFESTATIONS AS THE INFECTION PROGRESSES: § SOB, have noisy inspiration and expiration (inspiratory stridor and expiratory wheeze), purulent (pus-filled) sputum. IN SEVERE TRACHEOBRONCHITIS: § blood-streaked secretions may be expectorated ACUTE TRACHEOBRONCHITIS MEDICAL MANAGEMENT § Antibiotic treatment § Fluid intake § Suctioning and bronchoscopy may be needed to remove secretions. § In most cases, treatment of tracheobronchitis is largely symptomatic. § Cool vapor therapy or steam inhalations § Mild analgesics may be prescribed. ACUTE TRACHEOBRONCHITIS NURSING MANAGEMENT § Encourage bronchial hygiene, such as increased fluid intake and directed coughing to remove secretions. § Encourages and assists the patient to sit up frequently. § Follow proper medication regimen. § Caution patient against overexertion § Provide adequate rest. PNEUMONIA § an inflammation of the lung parenchyma caused by various microorganisms. § Pneumonitis is a more general term that describes an inflammatory process in the lung tissue that may predispose or place the patient at risk for microbial invasion. PNEUMONIA CLASSIFICATION CLASSIFIED INTO FOUR TYPES: § COMMUNITY-ACQUIRED PNEUMONIA (CAP) § HEALTH CARE–ASSOCIATED PNEUMONIA (HCAP) § HOSPITAL-ACQUIRED PNEUMONIA (HAP) § VENTILATOR-ASSOCIATED PNEUMONIA (VAP) PNEUMONIA PATHOPHYSIOLOGY Pneumonia arises from: § normal flora present in patients whose resistance has been altered § from aspiration of flora present in the oropharynx § acute or chronic underlying § bloodborne organisms that enter the pulmonary circulation PNEUMONIA GENERAL PATHOPHYSIOLOGY Pathogenic Agent triggers an inflammatory reaction in the alveoli exudate formation interferes with pulmonary diffusion PNEUMONIA GENERAL PATHOPHYSIOLOGY WBCs also migrate to the alveoli alveolar mucosal edema partial occlusion of the bronchi or alveoli decrease in alveolar oxygen tension V/Q mismatch hypoventilation PNEUMONIA GENERAL PATHOPHYSIOLOGY Venous blood passes through under ventilated alveolus Mixing of de-oxygenated & oxygenated blood to the system ARTERIAL HYPOXEMIA PNEUMONIA § Lobar pneumonia – If a substantial portion of one or more lobes is involved. § Bronchopneumonia is distributed in a patchy fashion COMMUNITY-ACQUIRED PNEUMONIA § a common infectious disease § occurs either in the community setting or within the first 48 hours after hospitalization or institutionalization. COMMUNITY-ACQUIRED PNEUMONIA CAUSATIVE AGENT S. pneumoniae (pneumococcus) § is the most common cause of CAP in people younger than 60 years without comorbidity and in those 60 years and older with comorbidity. COMMUNITY-ACQUIRED PNEUMONIA CAUSATIVE AGENT H. influenzae § causes a type of CAP that frequently affects older adults and those with comorbid illnesses (e.g., chronic obstructive pulmonary disease [COPD], alcoholism, and diabetes). COMMUNITY-ACQUIRED PNEUMONIA CAUSATIVE AGENT Mycoplasma pneumonia (M. pneumoniae) § is spread by infected respiratory droplets through person-to-person contact. COMMUNITY-ACQUIRED PNEUMONIA § Viruses are the most common cause of pneumonia in infants and children but are relatively uncommon causes of CAP in adults. § In immunocompromised adults, cytomegalovirus is the most common viral pathogen, followed by herpes simplex virus, adenovirus, and respiratory syncytial virus. HEALTH CARE–ASSOCIATED PNEUMONIA § An important distinction of HCAP is that the causative pathogens are often MDR. § Because HCAP is often difficult to treat, initial antibiotic treatment must not be delayed. HEALTH CARE–ASSOCIATED PNEUMONIA § HAP develops 48 hours or more after admission. § Certain factors may predispose patients to HAP because of: ü impaired host defenses, a variety of comorbid conditions, supine positioning and aspiration, coma, malnutrition, prolonged hospitalization, etc. HEALTH CARE–ASSOCIATED PNEUMONIA CAUSATIVE AGENTS § Enterobacter species § Klebsiella species § Escherichia coli § Proteus § H. influenzae § Serratia marcescens § Pseudomonas aeruginosa § Methicillin-sensitive or methicillin-resistant staphylococcus aureus (MRSA) § S. pneumoniae VENTILATOR–ASSOCIATED PNEUMONIA § Endotracheally intubated and has received mechanical ventilatory support for at least 48 hours. § The incidence of VAP increases with the duration of mechanical ventilation. ASPIRATION PNEUMONIA § refers to the pulmonary consequences resulting from entry of endogenous or exogenous substances into the lower airway. § The most common form of aspiration pneumonia is bacterial infection from aspiration of bacteria that normally reside in the upper airways. COVID-19 PNEUMONIA § a community-acquired coronavirus whose primary pathologic evolution occurs within the respiratory system. GENERAL MANIFESTATIONS § SpO2 ≤93% on room air § Tachypnea § Dyspnea § Asymptomatic (some patients) COVID-19 PNEUMONIA MANIFESTATIONS & FINDINGS: MILD COVID-19 § Fever § Nausea & vomiting § Nonproductive cough § Diarrhea § Sore throat § Anosmia (loss of smell) § Fatigue § Ageusia (loss of taste) § Myalgias (muscle aches) § Nasal congestion COVID-19 PNEUMONIA PATHOPHYSIOLOGY: VIRAL MULTIPLICATION Causative Agent: SARS-CoV-2 ACE2 receptors are particularly abundant in SARS-CoV-2 enters host type II alveolar and cells through ACE2 cellular vascular endothelial cells surface receptors within the pulmonary vascular circuit COVID-19 PNEUMONIA DIAGNOSIS & LAB FINDINGS § Bilateral nasal swabbing ü for viral antigen or nucleic acid § Leukopenia (low white blood cell count) § Lymphopenia (low lymphocyte count) § Elevated CK, LDH, CRP, ferritin § D-dimer levels § Chest x-ray findings (diffuse, bilateral, “ground-glass” opacities) COVID-19 PNEUMONIA TRANSMISSION § Viral Transmission: direct person-to-person contact via respiratory droplets § Fomite Transmission GENERAL MANAGEMENT § Supplemental oxygen (perhaps with ET intubation and mechanical ventilation) COVID-19 PNEUMONIA GENERAL MANAGEMENT MILD COVID-19 § Managed on an outpatient basis within their homes (Home Quarantine) ü conserves hospital resources ü diminishes likelihood of exposure to others, including HCW COVID-19 PNEUMONIA THERAPEUTIC REGIMEN § rest, hydrate, take antipyretic agents (e.g., acetaminophen) and monitor their symptoms. UNDER INVESTIGATION THERAPIES § Interleukin-6 (IL-6) antagonists (e.g., Tocizilumab) ü used for “cytokine storm” in severe COVID-19 § Convalescent Plasma ü transfuses antibodies from patients recovered from COVID-19 into patients with severe disease COVID-19 PNEUMONIA UNDER INVESTIGATION THERAPIES § Antiviral Agent ü Remdesivir COMPLICATIONS § Acute Respiratory Distress Syndrome (ARDS) ü commonly managed with ET intubation and mechanical ventilation COVID-19 PNEUMONIA Reportedly, many patients deteriorate rapidly and without clear prodromal clinical indicators from moderate to severe disease (Cascella et al., 2020) PNEUMONIA PNEUMONIA IN THE IMMUNOCOMPROMISED HOST: § Pneumocystis pneumonia (PCP), fungal pneumonias, and Mycobacterium tuberculosis. § Pneumonia in immunocompromised hosts may be caused by the organisms also observed in CAP or HAP (S. pneumoniae, S. aureus, H. influenzae, P. aeruginosa, M. tuberculosis). PNEUMONIA PREVENTION § Pneumococcal Vaccination § There are two types of pneumococcal vaccine recommended for adults: § pneumococcal conjugate vaccine (PCV13) § pneumococcal polysaccharide vaccine (PPSV23) PNEUMONIA MEDICAL MANAGEMENT Pharmacologic Therapy § Antibiotics § Suspected HAP à Broad spectrum IV antibiotic § Antipyretics § Decongestants PNEUMONIA MEDICAL MANAGEMENT Other Therapeutic Regimen § Hydration § Warm, moist inhalations § Bed rest § Oxygen, if needed. § ET, Mech Vent (complications) PNEUMONIA COMPLICATIONS § Shock and Respiratory Failure § Pleural Effusion ASPIRATION § inhalation of foreign material (e.g., oropharyngeal or stomach contents) into the lungs. § It is a serious complication that can cause pneumonia. ASPIRATION PATHOPHYSIOLOGY § the volume and character of the aspirated contents. § Aspiration pneumonia develops after inhalation of colonized oral or pharyngeal material. § The pathologic process involves an acute inflammatory response to bacteria and bacterial products. § Aspiration of solid food particles – mechanical blockage of the airways and secondary infection. ASPIRATION PREVENTION § RISK – level of consciousness of the patient. § Prevention is the primary goal when caring for patients at risk for aspiration (AACN, 2016) ASPIRATION PREVENTION § Compensating for Absent Reflexes § Assessing Feeding Tube Placement § Identifying Delayed Stomach Emptying § Managing Effects of Prolonged Intubation LUNG ABSCESS § A lung abscess is a localized collection of pus caused by microbial infection. § At risk individuals: ü impaired cough reflexes ü CNS disorders ü Drug addiction, alcoholism ü Esophageal disease, compromised immune function LUNG ABSCESS PATHOPHYSIOLOGY § Complication of bacterial pneumonia or are caused by aspiration of oral anaerobes into the lung. § may occur secondary to: § mechanical or functional obstruction of the bronchi by a tumor, foreign body, or bronchial stenosis, or from necrotizing pneumonias, TB, pulmonary embolism (PE), or chest trauma. LUNG ABSCESS PATHOPHYSIOLOGY § The site of the lung abscess is related to gravity and is determined by position. § most common areas for patients who are confined to bed. § Posterior segment of an upper lobe § Superior segment of the lower lobe LUNG ABSCESS PATHOPHYSIOLOGY § Eventually, the abscess becomes surrounded, or encapsulated, by a wall of fibrous tissue. § If the bronchus is involved, the purulent contents are expectorated continuously in the form of sputum. § If the pleura is involved, the result is an empyema. LUNG ABSCESS PATHOPHYSIOLOGY § A communication or connection between the bronchus and pleura is known as a bronchopleural fistula. LUNG ABSCESS CLINICAL MANIFESTATIONS § Most patients have a fever and a productive cough with moderate to copious amounts of foul- smelling, sometimes bloody, sputum. § Leukocytosis may be present. § Pleurisy or dull chest pain, dyspnea, weakness, anorexia, and weight loss are common. LUNG ABSCESS ASSESSMENT AND DIAGNOSTIC FINDINGS § Dullness on percussion and decreased or absent breath sounds with an intermittent pleural friction rub (grating or creaking sound) on auscultation. § Crackles may be present. LUNG ABSCESS ASSESSMENT AND DIAGNOSTIC FINDINGS § The chest x-ray reveals an infiltrate with an air– fluid level. § A computed tomography (CT) scan of the chest may be required to provide more detailed images of different cross-sectional areas of the lung. LUNG ABSCESS PREVENTION § Appropriate antibiotic therapy before any dental procedures in patients who must have teeth extracted while their gums and teeth are infected § Adequate dental and oral hygiene. § Appropriate antimicrobial therapy for patients with pneumonia. LUNG ABSCESS MEDICAL MANAGEMENT § Adequate drainage of the lung abscess § Postural drainage and chest physiotherapy. § A diet high in protein and calories is necessary, § Pulmonary resection (lobectomy) is performed if massive hemoptysis occurs or if there is little or no response to medical management. LUNG ABSCESS MEDICAL MANAGEMENT § IV antimicrobial therapy § Clindamycin (Cleocin) § Ampicillin-sulbactam (Unasyn) § Carbapenem § Treatment with IV antibiotics may continue for 3 weeks and longer. § IV antibiotics are discontinued, and oral administration of antibiotic therapy is continued for an additional 4 to 12 weeks and sometimes longer. LUNG ABSCESS NURSING MANAGEMENT § Administer antibiotics and IV treatments as prescribed. § Monitor drug adverse effects. § Chest physiotherapy is initiated as prescribed to facilitate drainage of the abscess. § Educate the patient to perform deep-breathing and coughing exercises. § Encourage a diet that is high in protein and calories. § Offer emotional support. END OF PART 1 MANAGEMENT OF PATIENTS WITH CHEST AND LOWER RESPIRATORY TRACT DISORDERS part 2 Professor: Joseph Christian G. Bacleon, RN  TABLE OF CONTENTS INFLAMMATORY AND INFECTIOUS PULMONARY DISORDERS PART 2 PULMONARY TUBERCULOSIS SARCOIDOSIS  TABLE OF CONTENTS PLEURAL DISORDERS PLEURISY EMPYEMA PLEURAL EFFUSION  TABLE OF CONTENTS ACUTE RESPIRATORY FAILURE ACUTE RESPIRATORY DISTRESS SYNDROME  TABLE OF CONTENTS PULMONARY VASCULAR DISORDERS PULMONARY EDEMA (NON-CARDIOGENIC) PULMONARY HYPERTENSION PULMONARY EMBOLISM  TABLE OF CONTENTS OCCUPATIONAL LUNG DISEASE: PNEUMOCONIOSES SILICOSIS ASBESTOSIS COAL WORKER’S PNEUMOCONIOSIS  TABLE OF CONTENTS CHEST TRAUMA BLUNT TRAUMA - Sternal and Rib Fractures - Flail Chest - Pulmonary Contusion PENETRATING TRAUMA PNEUMOTHORAX - Simple Pneumothorax - Traumatic Pneumothorax - Tension Pneumothorax  TABLE OF CONTENTS CARDIAC TAMPONADE SUBCUTANEOUS EMPHYSEMA INFLAMMATORY AND INFECTIOUS PULMONARY DISORDERS PULMONARY TUBERCULOSIS § is an infectious disease that primarily affects the lung parenchyma. § It also may be transmitted to other parts of the body, including the meninges, kidneys, bones, and lymph nodes. § Primary Causative Agent ü M. tuberculosis PULMONARY TUBERCULOSIS TRANSMISSION AND RISK FACTORS § Airborne transmission § An infected person releases droplet nuclei (usually particles 1 to 5 mcm in diameter) through talking, coughing, sneezing, laughing, or singing. PATHOPHYSIOLOGY: Initial Infection (2-10 weeks after exposure) transmitted through the airways to the alveoli deposited in the alveoli and bacteria are also transported begins to multiply via the blood & lymph system Mycobacterium (via inhalation) inflammatory reaction kidneys, bones, cerebral stimulation cortex PATHOPHYSIOLOGY: Initial Infection (2-10 weeks after exposure) Activation of phagocytes (neutrophils & macrophages) TB-specific lymphocytes lyse (destroy) the bacilli and normal tissue Tissue reaction (accumulation of exudate in alveoli) BRONCHOPNEUMONIA PATHOPHYSIOLOGY: Initial Infection (2-10 weeks after exposure) new tissue masses (from live and dead bacilli) surrounded by macrophages GRANULOMAS (forms a protective wall) GHON TUBERCLE transformed to a fibrous tissue mass (central portion of the mass) mass becomes necrotic forming a cheesy mass mass is calcified & forms a collagenous scar DORMANT PHASE (bacteria become dormant) PATHOPHYSIOLOGY: RE-ACTIVATION IMMUNOCOMPROMISED STATE TB REINFECTION ACTIVATION OF DORMANT BACTERIA GHON TUBERCLE ulcerates releasing the cheesy material into the bronchi bacteria then becomes airborne further spread of the disease ulcerated tubercle heals and forms scar tissue PATHOPHYSIOLOGY: RE-ACTIVATION further inflammation of the infected lung BRONCHOPNEUMONIA & TUBERCLE FORMATION (further development) UNTREATED spreads slowly downward to the hilum of the lungs extends to adjacent lobes TB REACTIVATION (adult-type progressive TB) TB GRANULOMA ANATOMY PULMONARY TUBERCULOSIS CLINICAL MANIFESTATIONS § The signs and symptoms of pulmonary TB are insidious. § Most patients have a low-grade fever, cough, night sweats, fatigue, and weight loss. § Hemoptysis also may occur. PULMONARY TUBERCULOSIS ASSESSMENT AND DIAGNOSTIC FINDINGS § positive skin test, blood test, or sputum culture for acid-fast bacilli § complete history, physical examination, tuberculin skin test, chest x- ray, and drug susceptibility testing. PULMONARY TUBERCULOSIS TUBERCULIN SKIN TEST § Mantoux method/test § Tubercle bacillus extract (tuberculin), purified protein derivative (PPD), is injected into the intradermal layer. § Test result is read 48 to 72 hours after injection. PULMONARY TUBERCULOSIS TUBERCULIN SKIN TEST § A reaction of 0 to 4 mm is considered not significant. § A reaction of 5 mm or greater may be significant in people who are at risk. § An induration of 10 mm or greater is usually considered significant in people who have normal or mildly impaired immunity. PULMONARY TUBERCULOSIS TUBERCULIN SKIN TEST A significant (positive) reaction does not necessarily mean that active disease is present in the body. A nonsignificant (negative) skin test means the person’s immune system did not react to the test. PULMONARY TUBERCULOSIS ADDITIONAL TEST § QuantiFERON-TB Gold® In-Tube and T-SPOT® § Sputum Culture ü A sputum specimen may be used to screen for TB. PULMONARY TUBERCULOSIS MEDICAL MANAGEMENT § Treated primarily with Anti-TB drugs for 6 to 12 months. § Several types of drug resistance must be considered when planning effective therapy: ü Primary drug resistance ü Secondary or acquired drug resistance ü Multidrug resistance PULMONARY TUBERCULOSIS MEDICAL MANAGEMENT R – Rifampicin I – Isoniazid P – Pyrazinamide E – Ethambutol S – Streptomycin First-Line Antituberculosis Medications for Active Disease PULMONARY TUBERCULOSIS MEDICAL MANAGEMENT § INH as prophylaxis for: ü Household family members of patients with active disease ü Patients with HIV infection who have a PPD test reaction with 5 mm of induration or more PULMONARY TUBERCULOSIS MEDICAL MANAGEMENT § Patients with fibrotic lesions suggestive of old TB detected on a chest x-ray and a PPD reaction with 5 mm of induration or more § Patients whose current PPD test results show a change from former test results, suggesting recent exposure to TB and possible infection (skin test converters) PULMONARY TUBERCULOSIS MEDICAL MANAGEMENT § Users of IV/injection drugs who have PPD test results with 10 mm of induration or more § Patients with high-risk comorbid conditions and a PPD result with 10 mm of induration or more. PULMONARY TUBERCULOSIS NURSING MANAGEMENT § Promoting airway clearance § Advocating adherence to the treatment regimen § Promoting activity and nutrition § Preventing transmission SARCOIDOSIS § is a type of interstitial lung disease. § inflammatory, multisystem, granulomatous disease of unknown etiology GRANULOMA: a noninfectious organized collection of macrophages that appear as a nodule. SARCOIDOSIS PATHOPHYSIOLOGY EXOGENOUS AGENTS HYPERSENSITIVITY RESPONSE OF THE BODY (bacteria, fungi, virus, chemicals) INFLAMMATION FORMATION OF A NONCASEATING GRANULOMA a noninfectious organized GRANULOMA INFILTRATION & FIBROSIS FORMATION collection of macrophages that appear as a nodule. LOW LUNG COMPLIANCE, IMPAIRED DIFFUSING CAPACITY, AND REDUCED LUNG VOLUMES SARCOIDOSIS CLINICAL MANIFESTATIONS Ø Hallmarks of sarcoidosis are its insidious onset and lack of prominent clinical signs or symptoms. Ø The lung is most commonly involved. GENERAL: § Dyspnea, cough, hemoptysis, and congestion SARCOIDOSIS CLINICAL MANIFESTATIONS OTHER s/sx: § uveitis; joint pain; fever; and granulomatous lesions of the skin, liver, spleen, kidney, and central nervous system. MULTISYSTEM INVOLVEMENT: § anorexia, fatigue, and weight loss The granulomas may disappear or gradually convert to fibrous tissue. SARCOIDOSIS ASSESSMENT and DIAGNOSTIC FINDINGS § Chest x-rays and CT scans are used to assess pulmonary adenopathy. § A mediastinoscopy or transbronchial biopsy may be used to confirm the diagnosis. § Diagnosis is confirmed by a biopsy that shows noncaseating granulomas. SARCOIDOSIS MEDICAL MANAGEMENT § Many patients undergo remission without specific treatment. § Corticosteroids ü Oral corticosteroids  PLEURAL CONDITIONS PLEURISY (PLEURITIS) § refers to inflammation of both layers of the pleurae (parietal and visceral) § May develop in conjunction with: § pneumonia or an upper respiratory tract infection, TB, or collagen disease, And others. PLEURISY (PLEURITIS) CLINICAL MANIFESTATIONS § The key characteristic of pleuritic pain is its relationship to respiratory movement. ü Taking a deep breath, coughing, or sneezing worsens the pain. § Pleuritic pain is limited in distribution rather than diffuse; it usually occurs only on one side. § Results to severe, sharp, knifelike pain. PLEURISY (PLEURITIS) ASSESSMENT AND DIAGNOSTIC FINDINGS § In the early period, when little fluid has accumulated, a pleural friction rub can be heard with the stethoscope. § Diagnostic tests may include chest x-rays, sputum analysis, thoracentesis to obtain a specimen of pleural fluid for examination, and, less commonly, a pleural biopsy. PLEURISY (PLEURITIS) MEDICAL MANAGEMENT § The objectives of treatment are: § to discover the underlying condition causing the pleurisy § to relieve the pain § Prescribed analgesic agents and topical applications of heat or cold provide symptomatic relief. PLEURISY (PLEURITIS) MEDICAL MANAGEMENT § A nonsteroidal anti-inflammatory drug may provide pain relief. PLEURISY (PLEURITIS) NURSING MANAGEMENT § Turning frequently onto the affected side to splint the chest wall and reduce the stretching of the pleurae. § Educate the patient to use the hands or a pillow to splint the rib cage while coughing. PLEURAL EFFUSION § a collection of fluid in the pleural space § it is usually secondary to other diseases. § Pleural effusion may be a complication of: ü heart failure, TB, pneumonia, pulmonary infections (particularly viral infections), nephrotic syndrome, connective tissue disease, PE and neoplastic tumors. PLEURAL EFFUSION PATHOPHYSIOLOGY: § The effusion can be a relatively clear fluid, or it can be bloody or purulent. § An effusion of clear fluid may be a transudate or an exudate. PLEURAL EFFUSION PATHOPHYSIOLOGY § A transudate (filtrate of plasma that moves across intact capillary walls) usually by imbalances in hydrostatic or oncotic pressures. § A transudative effusion most commonly results from heart failure. § An exudate (extravasation of fluid into tissues or a cavity) usually results from inflammation by bacterial products or tumors involving the pleural surfaces. PLEURAL EFFUSION CLINICAL MANIFESTATIONS § Usually, the clinical manifestations are caused by the underlying disease. § Pneumonia causes fever, chills, and pleuritic chest pain. § Malignant effusion may result in dyspnea, difficulty lying flat, and coughing. PLEURAL EFFUSION CLINICAL MANIFESTATIONS § A large pleural effusion causes dyspnea (shortness of breath). § A small-to-moderate pleural effusion causes minimal or no dyspnea. PLEURAL EFFUSION ASSESSMENT AND DIAGNOSTIC FINDINGS § Decreased or absent breath sounds. § Decreased fremitus § Dull, flat sound on percussion. § Tracheal deviation away from the affected side may also be apparent. § Physical examination, chest x-ray, chest CT, and thoracentesis confirm the presence of fluid. PLEURAL EFFUSION ASSESSMENT AND DIAGNOSTIC FINDINGS Pleural fluid is analyzed by: § Bacterial culture § Gram stain, AFB stain (for TB) § Red and white blood cell counts § Chemistry studies (glucose, amylase, lactate dehydrogenase, and protein) § Cytologic analysis for malignant cells, and ph. PLEURAL EFFUSION MEDICAL MANAGEMENT The objectives of treatment are: § to discover the underlying cause of the pleural effusion § to prevent re-accumulation of fluid § to relieve discomfort, dyspnea, and respiratory compromise. PLEURAL EFFUSION MEDICAL MANAGEMENT § Specific treatment is directed at the underlying cause (e.g., heart failure, pneumonia, and cirrhosis). § If the pleural fluid is an exudate, more extensive diagnostic procedures are performed to determine the cause. PLEURAL EFFUSION MEDICAL MANAGEMENT § Thoracentesis is performed: ü to remove fluid, to obtain a specimen for analysis ü to relieve dyspnea and respiratory compromise PLEURAL EFFUSION MEDICAL MANAGEMENT § Chest tube connected to a water-seal drainage system or suction to evacuate the pleural space and re-expand the lung. PLEURAL EFFUSION MEDICAL MANAGEMENT § Chemical pleurodesis may be performed to obliterate the pleural space and prevent re-accumulation of fluid. § Pleurodesis may be performed using either a thoracoscopic approach or a chest tube. PLEURAL EFFUSION MEDICAL MANAGEMENT § Surgical pleurectomy § Pleuroperitoneal shunt PLEURAL EFFUSION NURSING MANAGEMENT § Prepares and position the patient for thoracentesis and offers support throughout the procedure. § Record amount of thoracentesis fluid drained and sent sample for appropriate laboratory testing. § Monitoring the water-sealed system for CTT. § Record the amount of drainage at prescribed intervals. EMPYEMA § An empyema is an accumulation of thick, purulent fluid within the pleural space, often with fibrin development and a loculated (walled-off) area where infection is located. EMPYEMA PATHOPHYSIOLOGY § Most empyemas occur as complications of bacterial pneumonia or lung abscess. encloses the pleural fluid is lung within a thin (with a low low leukocyte fibropurulent thick exudative leukocyte count stage membrane count) (loculated empyema) EMPYEMA CLINICAL MANIFESTATION § Fever, night sweats, pleural pain, cough, dyspnea, anorexia, weight loss § If the patient is immunocompromised, the symptoms may be vague. § If the patient has received antimicrobial therapy, the clinical manifestations may be less obvious. EMPYEMA ASSESSMENT AND DIAGNOSTIC FINDINGS § Decreased or absent breath sounds over the affected area. § Dullness on chest percussion. § Decreased fremitus. § The diagnosis is established by chest CT. § Usually, a diagnostic thoracentesis is performed, often under ultrasound guidance. EMPYEMA MEDICAL MANAGEMENT § The objectives of treatment: § to drain the pleural cavity § to achieve complete expansion of the lung. § Drainage of Fluid § Antibiotics (primarily by IV route) EMPYEMA MEDICAL MANAGEMENT Drainage of the pleural fluid: § Needle aspiration (thoracentesis) § Tube thoracostomy § Open chest drainage via thoracotomy EMPYEMA MEDICAL MANAGEMENT § This exudate must be removed surgically (decortication). § The drainage tube is left in place until the pus-filled space is obliterated completely. Decortication EMPYEMA NURSING MANAGEMENT § Help the patient cope with the condition. § Instruct the patient in lung-expanding breathing exercises. § Provide care specific to the method of drainage of the pleural fluid. § Instruct the patient and family on care of the drainage system and drain site, measurement and observation of drainage, signs and symptoms of infection, and how and when to contact the primary provider. ACUTE RESPIRATORY FAILURE (ARF) § a sudden and life-threatening deterioration of the gas exchange function of the lung § indicates failure of the lungs to provide adequate oxygenation or ventilation for the blood. ACUTE RESPIRATORY FAILURE (ARF) § Decrease PaO2 (50 mmHg) → hypercapnia § Arterial pH of (