pediagenosis: Respiratory
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Showing posts with label Respiratory. Show all posts
Showing posts with label Respiratory. Show all posts

Monday, February 15, 2021

LYMPHANGIOLEIOMYOMATOSIS

LYMPHANGIOLEIOMYOMATOSIS

LYMPHANGIOLEIOMYOMATOSIS

Pulmonary lymphangioleiomyomatosis (LAM) is a diffuse, progressive lung disease that affects young women of childbearing age. It occurs as a sporadic disease (S-LAM) or with a tuberous sclerosis complex (TSC-LAM). The incidence and prevalence (two to five per million) of sporadic LAM are unknown. Whites are afflicted much more commonly than other racial groups.

IDIOPATHIC PULMONARY HEMOSIDEROSIS

IDIOPATHIC PULMONARY HEMOSIDEROSIS

IDIOPATHIC PULMONARY HEMOSIDEROSIS

Idiopathic pulmonary hemosiderosis (IPH) is a disease of unknown origin, usually occurring in children, equally in both genders. Repeated episodes of pulmonary hemorrhage with resultant blood-loss anemia and eventual respiratory failure characterize the illness. In children, this disorder is associated with celiac disease and elevated IgA levels. Environmental exposure to molds, particularly Stachybotrys chartarum, has been suggested as a causative factor in infants with IPH, but the relationship remains unproven.

PULMONARY ALVEOLAR PROTEINOSIS

PULMONARY ALVEOLAR PROTEINOSIS

PULMONARY ALVEOLAR PROTEINOSIS

Pulmonary alveolar proteinosis (PAP) is an uncommon disease characterized by filling of alveoli with a lipoproteinaceous material composed principally of the phospholipid surfactant and surfactant apoproteins. This amorphous material stains with periodic acid–Schiff (PAS) reagent. Impaired processing of surfactant by alveolar macrophages and diminished granulocyte macrophage-colony stimulating factor (GM-CSF) protein levels or function contributes to the pathogenesis of PAP. There is little inflammatory reaction in the surrounding lung, and the underlying lung architecture is preserved.

CRYPTOGENIC ORGANIZING PNEUMONIA

CRYPTOGENIC ORGANIZING PNEUMONIA

CRYPTOGENIC ORGANIZING PNEUMONIA

Cryptogenic organizing pneumonitis (COP) is a specific clinicopathologic syndrome of unknown cause. The incidence and prevalence of COP are unknown, but a cumulative incidence of six to seven per 100,000 hospital admissions was found at a major teaching hospital. The disease onset is typically in the fifth or sixth decades of life, with men and women being affected equally.

IDIOPATHIC INTERSTITIAL PNEUMONIAS

IDIOPATHIC INTERSTITIAL PNEUMONIAS

IDIOPATHIC INTERSTITIAL PNEUMONIAS

The idiopathic interstitial pneumonias (IIPs) are a subset of the acute and chronic lung disorders collectively referred to as interstitial lung diseases (ILDs) or diffuse parenchymal lung diseases. In 2002, the American Thoracic Society/European Respiratory Society consensus classification separated the IIPs into seven clinical-radiologic-pathologic entities: idiopathic pulmonary fibrosis (IPF), idiopathic nonspecific interstitial pneumonia (NSIP), respiratory bronchiolitis–associated ILD/desquamative interstitial pneumonia (RB-ILD/DIP), cryptogenic organizing pneumonia (COP), acute interstitial pneumonia (AIP), and lymphoid interstitial pneumonia (LIP). The various sub-groups of the IIPs are often clinically indistinguishable (with the exception of COP and AIP).

ACUTE LUNG INJURY

ACUTE LUNG INJURY

ACUTE LUNG INJURY

The syndrome now referred to as acute lung injury (ALI) is a condition defined by noncardiogenic pulmonary edema, originally described almost 50 years ago as Da Nang lung and subsequently as acute or adult respiratory distress syndrome (ARDS). The commonly used definition of ALI includes four elements: acute onset of symptoms, bilateral alveolar infiltrates on chest radiography, a PaO2 (partial pressure of oxygen)/FIO2 (fraction of inspired oxygen) ratio below 300 (200 defines the more severe subset of the patients as ARDS), and no evidence of left atrial hypertension. Histologically, the syndrome is identified by the classic finding of diffuse alveolar damage, but few patients undergo lung biopsy during the course of their clinical illness.

Saturday, January 30, 2021

RESPIRATORY DISTRESS SYNDROME

RESPIRATORY DISTRESS SYNDROME

RESPIRATORY DISTRESS SYNDROME

Respiratory distress syndrome (RDS) presents within 4 four hours of birth, usually in prematurely born infants. It used to be called hyaline membrane disease because hyaline membranes line the terminal airways of infants who are surfactant deficient. The hyaline membranes are formed by coagulation of plasma proteins that have leaked onto the lung surface through damaged capillaries and epithelial cells. The term hyaline membrane disease should only be used if there is histologic confirmation; therefore, the term RDS is now widely used.

DIAPHRAGMATIC INJURIES

DIAPHRAGMATIC INJURIES

DIAPHRAGMATIC INJURIES

The diaphragm is an arched muscle dividing the thorax and the abdomen and is interrupted by three major openings: the vena cava, esophagus, and aorta. The diaphragm is the main respiratory muscle, with inspiratory and expiratory functions. Diaphragmatic injuries may be caused by penetrating or blunt trauma; the mechanism influences the site and extent of injury. With gunshot wounds, the chances of right versus left side are roughly equal, and the wound from most hand- guns is small, usually smaller than 1 cm. In contrast, stab wounds involve the left side of the diaphragm more commonly because the right-handed assailant holds the weapon in the right hand and confronts the victim at close range. Knife wounds are also typically small, usually smaller than 2 cm. The left hemidiaphragm is injured two to three times more frequently than the right after blunt trauma. The difference is attributed to the protective effect of the liver that distributes a sudden increase in intraabdominal pressure more evenly across the right hemidiaphragm. Blunt diaphragm injuries are considerably larger than penetrating wounds and are usually larger than 5 cm in length and in many cases exceed 10 cm. During quiet respiration, the normal intraperitoneal pressures ranges from+2 to +10 cm H2O, and the corresponding intrapleural pressure fluctuates from -5 to -10 cm; thus, a gradient exists varying from +7 to +20 cm H2O. But with maximal inspiration, this gradient may exceed 100 cm H2O. Consequently, there is high risk for abdominal viscera to herniate into the thorax. The risk is higher on the left side because the liver provides a barrier on the right, and herniation increases with the extent of the diaphragmatic defect. Ambroise Paré, in 1579, is credited with describing the first case of visceral herniation in a French artillery captain who sustained a gunshot wound to the left chest 8 months before a lethal colonic obstruction.

TRAUMATIC ASPHYXIA

TRAUMATIC ASPHYXIA

TRAUMATIC ASPHYXIA

Traumatic asphyxia is a condition resulting from a severe sustained compressive force on the thorax. Ollivier is credited for the first autopsy description of a syndrome of cranial cyanosis, subconjunctival hemorrhage, and vascular engorgement of the head, which was observed in a person crushed to death by a panicked crowd in Paris. The syndrome was termed masque ecchymotique. This form of crush injury occurs in association with vehicle crashes, industrial accidents, uncontrolled crowd conditions and trampling, and any type of trauma characterized by a heavy object falling onto the chest, such as an individual working under a car that slips off the jack or a child pinned under a garage door. The syndrome is also seen with side wall collapse at an excavation site or may be seen with deep-sea divers from underwater explosions. The pathogenesis of traumatic asphyxia is attributed to a sudden compression of the heart between the anterior chest wall and vertebral column, generating a pressure surge in the right side of the heart that is decompressed by reverse blood flow into the superior vena cava and its major branches, which lack valves. The subsequent massive capillary engorgement and rupture throughout the head, neck, shoulders, and upper thorax results in stagnation of blood, which desaturates and results in the characteristic bluish discoloration of the skin. There may be intense swelling of the face and neck, as well as petechial hemorrhages of the skin of the face and conjunctiva. It is postulated that deep inspiration and transient airway obstruction exaggerate the superior vena cava hypertension. These events may occur as a reflex in the victim’s anticipating the impact.

Friday, January 29, 2021

TRACHEOBRONCHIAL RUPTURE

TRACHEOBRONCHIAL RUPTURE

TRACHEOBRONCHIAL RUPTURE

Rupture of the trachea or major bronchi is usually secondary to a nonpenetrating injury of the thorax resulting from a high-energy frontal impact motor vehicle crash. More than 80% of the ruptures are within 2.5 cm of the carina. The proposed mechanisms for this injury include (1) anteroposterior compression with subsequent widening of the transverse diameter that pulls the lungs apart, producing traction on the trachea at the carina; (2) compression of the trachea and major bronchi between the sternum and vertebral column in a patient with a closed glottis exceeds the elasticity of the membranous portion of the airway; and (3) rapid deceleration injury at a point of relative fixation of the carina produces shear forces. Tracheal lacerations usually occur at the junction of the membranous and cartilaginous trachea. Major bronchial rupture is typically unilateral and is more common on the right side. The severity of blunt trauma required for these tracheobronchial ruptures is usually associated with multi-system injuries of the head, abdomen, and extremities. The clinical presentation appears in two distinct patterns, depending on whether there is free communication between the airway rupture and the pleural cavity. If there is free communication, a large pneumothorax is present, and despite tube thoracostomy, there is a persistent vigorous air leak and the lung cannot be reexpanded. Dyspnea is prominent because of the loss of functioning lung. If there is no communication with the pleural cavity, the air escaping via the tracheobronchial injuries forms impressive mediastinal and subcutaneous emphysema. On auscultation, Hamman sign may be evident (i.e., a crunching sound synchronized with the heart beat caused by mediastinal emphysema). In both cases, there may be significant hemoptysis as well. Air embolism is also a life-threatening consequence that must be promptly treated by emergency thoracotomy with cross-clamping of the pulmonary hilum on the affected side.

PULMONARY LACERATION

PULMONARY LACERATION

PULMONARY LACERATION

Rapid deceleration from blunt thoracic trauma may produce shearing forces that lacerate the lung. Other causes include missiles, knives, and fractured ribs that directly lacerate the lung and lung hyperinflation from such causes as blast injuries and diving accidents. Lung lacerations usually manifest as hemopneumothoraxes requiring early tube thoracostomy. A persistent air leak is common but typically seals as the lung becomes fully reexpanded. With more extensive injuries requiring endotracheal intubation and positive-pressure ventilation, however, there is a risk of life-threatening acute bronchovenous air embolism. The typical scenario is a patient who is hypovolemic and requires semi-urgent endotracheal intubation for moderate hypoxemia but develops acute cardiac deterioration. As pressure in the airway is increased, air is forced from disrupted terminal bronchi into an adjacent injured pulmonary vein, which conveys the air bubbles into the left side of the heart and ultimately into the coronary or carotid systems. The hypovolemic patient is more susceptible to air embolism because of decreased pulmonary venous pressure, thus increasing the gradient from the airway. Symptomatic coronary air embolus mandates resuscitative thoracotomy with pulmonary hilar cross-clamping and vigorous internal cardiac massage. Air should be vented from the left ventricle and ascending aorta. Ongoing air leak from the injured lung is usually managed with staple tractotomy (i.e., linear stapling is performed on both sides of the torn lung as an alternative to anatomic resection). Pulmonary tractotomy is particularly useful when required for persistent air leaks from multiple lobes caused by a gunshot wound, avoiding the necessity for emergent pneumonectomy, which is often poorly tolerated because of right ventricular failure.

HEMOTHORAX

HEMOTHORAX

HEMOTHORAX

Hemothorax is bleeding into the pleural cavity; the source of bleeding can be from a variety of structures in the thorax or from the abdomen through a diaphragmatic injury. The most common cause of hemothorax after blunt trauma is the chest wall with disrupted parietal pleural allowing blood loss from torn intercostal vessels to enter the pleural cavity; after penetrating injuries, it is usually from the lung parenchyma. Persistent bleeding into the thorax suggests a systemic source, usually an intercostal or internal mammary artery, but occasionally a named thoracic vein (e.g., azygos, subclavian, or pulmonary) will produce ongoing blood loss. Typically, a hemothorax from a ruptured thoracic aorta, pulmonary artery, or heart is extensive at the time of emergency department arrival. Of note, occasionally, the source of major persistent bleeding in the thorax originates from the liver or spleen via an associated diaphragmatic injury.

Wednesday, January 6, 2021

PNEUMOTHORAX

PNEUMOTHORAX

PNEUMOTHORAX

Pneumothorax is a collection of air within the pleural space; after trauma, pneumothorax is most commonly caused by a rib fracture tearing the visceral pleura of the lung, allowing air to escape during inspiration. Penetrating injuries (e.g., stab wounds, gunshot wounds) also frequently produce a pneumothorax via this mechanism. In these cases of penetrating trauma, 80% of patients will also have blood in the pleural space. Pneumothorax is usually identified on chest radiographs, although it may also be seen during chest or abdominal computed tomography scanning or during ultrasound examination of the abdomen after trauma (focal assessment with sonography for trauma [FAST] examination).

FLAIL CHEST AND PULMONARY CONTUSION

FLAIL CHEST AND PULMONARY CONTUSION

FLAIL CHEST AND PULMONARY CONTUSION

Flail chest refers to instability of the chest wall caused by multiple segmented rib fractures or cartilage disruptions such that a portion of the bony chest wall loses its continuity from the remaining thoracic cage because of contiguous rib disruptions. A flail chest occurs in the setting of severe trauma, usually after a motor vehicle crash or fall from more than 20 feet. If the crushing blow is directly over the sternum, as with an impact by the steering column, the flail segment is produced by bilateral costochondral separations, and there may be an associated sternal fracture. Because of protective air bag systems in automobiles, however, lateral mid-chest flail segments are more common. In either location, it is evident on physical examination that the floating portion of the chest wall moves in and out with respiration in an opposite or paradoxical manner with respect to the remaining intact chest wall. This abnormality in ventilatory mechanics renders the respiratory effort inefficient and, when compounded by reduced tidal volume because of pain, may produce extensive lung collapse with hypoxia, hypercapnia, ineffective cough, and retention of secretions. Although the mechanical effects of a flail segment may appear impressive, the associated hypoxia is often exacerbated by underlying pulmonary contusion. Consequently, the management beyond pain control of flail chest is largely governed by the magnitude of concomitant pulmonary contusion. Although surgical stabilization of the chest wall for acute flail chest has been suggested in the past, randomized trials have not established an outcome benefit. Occasionally, a patient with persistent chest wall instability caused by nonunion will be a candidate for internal rib fixation with a plate. These patients include those with severe pain and respiratory compromise, typically caused by multiple, severely displaced rib fractures with overriding fragments.

RIB AND STERNAL FRACTURES

RIB AND STERNAL FRACTURES

RIB AND STERNAL FRACTURES

Thoracic injury is directly responsible for 25% of trauma deaths and contributes to the demise of another 25%. Most mortality directly attributable to chest trauma occurs in the prehospital setting, resulting from disruption of the great vessels, heart, or tracheobronchial tree. Of those who survive the initial insult, fewer than 15% sustain injury that necessitates operative intervention. Although tube thoracostomy is often the only procedure required initially for chest trauma, injuries to the thoracic cage and lung prolong hospitalization and may be the source of long-term morbidity and occasionally death.

CHYLOTHORAX

CHYLOTHORAX

CHYLOTHORAX

A chylothorax is defined as the accumulation of chyle in the pleural space that results from disruption of the thoracic duct or one of its major tributaries. A total of 1500 to 2500 mL of chyle empties into the venous system daily from the thoracic duct, depending on the fat content of the diet. The formation of chylomicrons occurs from long-chain triglycerides in dietary fats that are transported to the cisterna chyli, which overlie the anterior surface of the second lumbar vertebrae to the right and posterior to the aorta. Although there are multiple variations in the course of the thoracic duct, the usual pathway is through the aortic hiatus of the diaphragm into the posterior mediastinum. The thoracic duct most commonly crosses from the right side of the vertebral column to the left between the 7th and 5th thoracic vertebrae as it ascends posterior to the aortic arch and empties into the junction of the jugular and subclavian veins.

PLEURAL EFFUSION IN MALIGNANCY

PLEURAL EFFUSION IN MALIGNANCY

PLEURAL EFFUSION IN MALIGNANCY

The diagnosis of a malignant pleural effusion is established when malignant cells are identified in pleural fluid or in pleural tissue. However, in about 10% to 15% of patients with a known malignancy and a pleural effusion, malignant cells cannot be identified; these effusions are termed paramalignant effusions. Paramalignant effusions develop from local effects of the tumor (lymphatic obstruction), systemic effects of the tumor (pulmonary embolism), and complications of therapy (radiation pleuritis and effects of chemotherapy). Although carcinoma from any organ can metastasize to the pleura, lung cancer and breast carcinoma are responsible for approximately 60% of all malignant pleural effusions. Ovarian and gastric carcinoma are the third and fourth leading cancers to cause malignant effusions; lymphomas account for approximately 10% of all malignant pleural effusions.

Tuesday, January 5, 2021

PARAPNEUMONIC EFFUSION

PARAPNEUMONIC EFFUSION

PARAPNEUMONIC EFFUSION

A parapneumonic effusion is defined as pleural fluid that develops from pneumonia. Parapneumonic effusion is the most common cause of an exudative effusion. A practical, clinical classification of a parapneumonic effusion is as follows: (1) an uncomplicated parapneumonic effusion resolves with antibiotic therapy alone without pleural space sequelae; (2) a complicated para-pneumonic effusion requires pleural space drainage to resolve pleural sepsis and prevent progression to an empyema; and (3) empyema is the end-stage of a para-pneumonic effusion. Empyema is defined by its appearance, which is an opaque, whitish-yellow, viscous fluid (pus) that is generated from serum coagulation proteins, cellular debris, and fibrin deposition.

UNEXPANDABLE LUNG

UNEXPANDABLE LUNG

UNEXPANDABLE LUNG

An unexpandable lung may result from visceral pleural restriction, an endobronchial lesion, or chronic atelectasis. The most common causes of visceral pleural restriction are malignancy and infection; others include inflammatory pleurisy, such as rheumatoid disease, and coronary artery bypass graft (CABG) surgery.

PLEURAL EFFUSION IN HEART DISEASE

PLEURAL EFFUSION IN HEART DISEASE

PLEURAL EFFUSION IN HEART DISEASE

Pleural effusions commonly occur in patients with congestive heart failure (CHF). The effusions are a sequela of pulmonary venous hypertension and not the result of isolated systemic venous hypertension unless there is associated ascitic fluid with transdiaphragmatic movement into the pleural space. With systolic or diastolic left-sided heart failure, pulmonary venous pressure increases, causing fluid to move into the lung interstitium; the increased interstitial–pleural pressure gradient promotes the movement of fluid between mesothelial cells into the pleural space. If pleural fluid formation exceeds removal through the parietal pleural lymphatics, a pleural effusion will develop.

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