Atelectasis and Pulmonary Edema Lecture PDF

Atelectasis and Pulmonary Edema Eugen Petcu, MD, PhD Associate Professor Department of Biomedical Sciences [email protected] Session Objectives At the end of this session, you should be able to: 1. Discuss pathogenesis of Atelectasis and Respiratory Distress Syndrome in Newborns 2. Demonstrate an u...

Atelectasis and Pulmonary Edema Eugen Petcu, MD, PhD Associate Professor Department of Biomedical Sciences [email protected] Session Objectives At the end of this session, you should be able to: 1. Discuss pathogenesis of Atelectasis and Respiratory Distress Syndrome in Newborns 2. Demonstrate an understanding of the Hemodynamic Pulmonary Edema 3. As well as Microvascular Injury Associated Pulmonary Edema 4. Define and explain the Acute Respiratory Distress Syndrome (ARDS) Source: Course Syllabus  Atelectasis -incomplete expansion of the lungs (neonatal atelectasis) -collapse of previously inflated lung. Obstructive atelectasis: resorption atelectasis circulating blood will reabsorb the gas from alveoli (due to obstruction between alveoli and trachea) i.e., from foreign body, mucus plugs, or tumor Nonobstructive atelectasis: compression and contraction(cicatricial, cicatrization) atelectasis Compression: fluid or air in pleural cavity Contraction: pulmonary or pleural fibrosis prevents full lung expansion Clinical features Pain on the affected side as well as dyspnea Cyanosis and dullness to percussion over the involved area Diminished or absent breath sounds Reduced or absent chest excursion of the involved hemithorax May have tracheal deviation towards the affected side Diagnosis of atelectasis involves Treatment of atelectasis : the following: Chest physiotherapy - Postural drainage, chest wall percussion and Arterial blood gas evaluation vibration, a forced expiration technique (called huffing) Continuous positive airway pressure delivered via a nasal cannula or Chest radiographs and CT scans facemask Bronchodilators – to promote sputum expectoration Flexible fibreoptic bronchoscopy Surgical - Segmental resection or lobectomy (in cases of chronic atelectasis) Obstruction Atelectasis aka Resorption Atelectasis -excessive secretions (e.g., mucus plugs) -exudates within smaller bronchi: bronchial asthma, chronic bronchitis, bronchiectasis, and postoperative states. -aspiration of foreign bodies and intrabronchial tumors Obstruction of a lobar bronchus produces lobar atelectasis. Obstruction of a segmental bronchus is likely to produce segmental atelectasis. Obstruction/Resorption atelectasis pathogenesis After bronchial obstruction, the blood circulating in the alveolar-capillary membrane absorbs the gas from alveoli. Gas absorption from the alveoli promotes: retraction of the lung airless state within those alveoli. In the early stages, blood then perfuses the unventilated lung inducing arterial hypoxemia. Also, the alveolar spaces fill with secretions and cells preventing complete collapse of the atelectatic lung. The uninvolved surrounding lung tissue distends, displacing the surrounding structures. There is a mediastinal shift towards the atelectatic area, while the diaphragm is elevated, and the chest wall flattens. Compression Atelectasis Represents accumulation of fluid (transudate, exudate, or blood) a tumor, or air (pneumothorax) within the pleural cavity. It is seen in patients with elevated position of the diaphragm (bedridden patients, ascites, after surgery). Mediastinum and/or trachea deviated away from affected side Air increases overall transparency/lucency of hemithorax Hyperresonance on PE Contraction atelectasis: cicatrization/cicatricial It follows a reduction of lung volume subsequent to severe parenchymal scarring. This is described after granulomatous lung disease (TB) or necrotizing pneumonia. There is also fibrosis/scarring with narrowing of bronchial lumen. Macro: The left lung and the middle and the lower lobes of right lung are collapsed. The upper lobe of the right lung is not affected. https://pathology.or.jp/corepictures EN/05/c05/01.html Respiratory Distress Syndrome in Newborns: RDS, Neonatal Resp Distress Syndrome or Hyaline Membrane Disease It represents a special form of atelectasis due to loss of surfactant. Surfactant (lipids, proteins, glycoproteins, lecithin, sphingomyelin) is manufactured by type II pneumocytes and decreases surface tension in the small airways which preventing collapse on expiration Surfactant synthesis begins in-utero at 28th weeks and its abundant after 35th weeks. Women who must deliver their babies prematurely receive glucocorticoids in order to increase fetal surfactant synthesis, which reduces the potential for developing RDS Causes: Prematurity Complications Maternal diabetes Blindness Bronchopulmonary dysplasia Clinical Findings: Patent ductus arteriosus (PDA) The air spaces are lined by hyaline membranes made of Grunting, tachypnoea, Intraventricular hemorrhage fibrin and epithelial necrotic cells intercostal retractions Necrotizing enterocolitis https://pathology.or.jp/corepicturesEN/22/c06/01. Lecithin-to-sphingomyelin ratio Hypoglycemia html < 1.5 in RDS Pulmonary Edema It is excessive accumulation of fluid in the alveoli. Hemodynamic edema: an acute increase in left ventricular filling pressure and left atrial pressure which promotes an increased capillary hydrostatic pressure secondary to elevated pulmonary venous pressure: Causes associated with impaired left ventricular function coronary artery disease, hypertension valvular disease, dilated cardiomyopathy metabolic conditions (e.g., hypothyroidism) myocarditis, ventricular hypertrophy, outflow obstruction There is impaired left ventricular contractility and decreased cardiac output, which activates the renin-angiotensin- aldosterone and sympathetic nervous system, salt and water retention inducing peripheral and pulmonary edema. This type of edema is also caused by hypoalbuminemia which determines loss of oncotic pressure associated with edema: liver failure, protein losing-enteropathy and nephrotic syndrome.. Microvascular injury associated pulmonary edema It is caused by changes in capillary permeability as result of a direct or indirect insult acute respiratory distress syndrome, bacterial pneumonia, radiation, lung trauma, liquid aspiration high altitude:hypoxia, dyspnea, and dry cough when exposed to a high altitude opioid overdose, inhaled gases-oxygen injury Hemodynamic Pulmonary Edema Epidemiology 6 years mortality : 85% in those with congestive heart failure Males are typically affected more than female. The elderly are at a higher risk. Macroscopic The lungs are heavy, fluid-filled on cut section Edema accumulates initially in the basal This impairs ventilation and O2 regions of the lower lobes because diffusion creating a favourable hydrostatic pressure is greatest in these environment for bacteria sites (dependent edema). growth inducing pneumonia Clinical Patients cough up froth when the edema fluid escapes into the alveoli. Histology Hemodynamic Pulmonary Edema Left side image: the alveolar spaces are filed by an intra-alveolar transudate which pale pink and granular. Right side image: Dilated alveolar capillaries, alveolar microhemorrhages and hemosiderin-laden macrophages (“heart failure” cells) may be present. In long-standing pulmonary congestion (e.g., as seen in mitral stenosis), hemosiderin-laden macrophages are abundant, These changes not only impair respiratory function but also predispose to infection  Microvascular Injury Associated Pulmonary Edema and ARDS : Primary injury to the vascular endothelium or damage to alveolar epithelial cells (with secondary microvascular injury) produces an ARDS: inflammatory exudate into the interstitial space Acute and rapidly progressive and, in more severe cases, into the alveoli. hypoxia with bilateral pulmonary edema due to alveolar injury Injury-related alveolar edema is an important caused by pulmonary or systemic feature of a serious and often fatal condition, insults acute respiratory distress syndrome (ARDS) 40% die within 28 days from an onset of ARDS, mainly due to infection / sepsis and multiple organ dysfunction syndrome ARDS Clinical Features Profound dyspnea and tachypnea Respiratory failure, hypoxemia, cyanosis Respiratory acidosis Hypoxemia may be refractory to oxygen therapy due to ventilation- perfusion (V/Q) mismatch and decreased compliance Decreased PaO2/FiO2