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Torregosa, Cyrus Dan
I. Pleural Effusion
Pleural effusion is excess fluid that accumulates in the fluid-filled space that surrounds the lungs. Excessive amounts of such fluid can impair breathing by limiting the expansion of the lungs during inspiration. It is a rarely a primary disease process but is usually occurs secondary to other disease. Normally the pleural space contains a small amount of liquid (5-15 ml) which acts as a lubricant that allows the pleural surfaces to move without friction. Types of fluids Four types of fluids can accumulate in the pleural space:  Serous fluid (hydrothorax)  Blood (hemothorax)  Chyle (chylothorax)  Pus (pyothorax or empyema) 

Diagnosis
Effusion fluid often settles at the lowest space due to gravity. Pleural effusion is usually diagnosed on the basis of medical history and physical exam, and confirmed by chest x-ray. Once accumulated fluid is more than 500 ml, there are usually detectable clinical signs in the patient, such as decreased movement of the chest on the affected side, dullness to percussion over the fluid, diminished breath sounds on the affected side, decreased vocal resonance and fremitus (though this is an inconsistent and unreliable sign), and pleural friction rub. Above the effusion, where the lung is compressed, there may be bronchial breathing. 

Causes
Because pleural effusion formation is a manifestation of underlying disease as opposed to being a disease process in itself, many underlying etiologies may exist. Pleural effusions are generally classified as transudates or exudates, based on the mechanism of fluid formation and pleural fluid chemistry. Transudates result from an imbalance in oncotic and hydrostatic pressures, whereas exudates are the result of inflammation of the pleura or decreased lymphatic drainage. In some cases, the pleural fluid may have some characteristics of both transudatives and exudatives. The etiologic spectrum of pleural effusion is extensive. However, most pleural effusions are caused by congestive heart failure, pneumonia, malignancy, or pulmonary embolism. Transudates Systemic factors that govern formation of transudates include increased systemic and/or pulmonary capillary hydrostatic pressure (elevated pulmonary capillary wedge pressure of 10

cm H2 O or higher), decreased colloid osmotic pressure in the systemic circulation, or both. Pleural membranes are intact and are not involved in pathogenesis of the fluid formation. The permeability of pleural capillaries to proteins is normal. Conditions associated with transudate formation include the following: o Congestive heart failure o Cirrhosis o Nephrotic syndrome o Urinothorax (usually due to obstructive uropathy) o Myxedema o Cerebrospinal fluid leaks to the pleura (generally in the setting of ventriculopleural shunting, or trauma or surgery to the thoracic spine) o Peritoneal dialysis o Duropleural fistula (rare but may be a complication of spinal cord surgery) o Extravascular migration of central venous catheter Exudates Local factors governing formation of exudates include altered permeability of pleural membranes, increased capillary wall permeability or vascular disruption, and decreased or complete obstruction of lymphatic drainage of pleural space. Pleural membranes are involved in pathogenesis of the fluid formation. Permeability of pleural capillaries to proteins is high, resulting in elevated protein content. Conditions associated with exudates formation include the following: Malignancy (most commonly lung or breast cancer, lymphoma, and leukemia; less commonly ovarian carcinoma, stomach cancer, sarcomas, melanoma) o Pneumonia (often associated with treatment failure) o Tuberculosis o Pulmonary embolism o Fungal infection o Pancreatic pseudocyst o Intra-abdominal abscess o Status-post coronary artery bypass graft surgery o Postcardiac injury syndrome o Pericardial disease o Rheumatoid pleuritis o Systemic lupus erythematosus o Asbestos-related pleural disease o Uremia o Trapped lung (localized pleural scarring with the formation of a fibrin peel prevents incomplete lung expansion, at times leading to pleural effusion) o Extravascular migration of central venous catheter o Fistula (pancreaticopleural, ventriculoperitoneal, ventriculopleural, biliopleural, gastropleural) 

Signs and Symptoms
The clinical manifestations of pleural effusion are variable and often are related to the underlying disease process. The most commonly associated symptoms are progressive dyspnea, cough, and pleuritic chest pain. y Dyspnea o Dyspnea is the most common symptom at presentation and generally indicates the presence of a large effusion. o It is reported to occur in 50% of patients with malignant pleural effusions. o Other factors (eg, underlying lung disease, cardiac dysfunction, anemia) may also contribute to the development of dyspnea. y Chest pain o Chest pain in this setting results from pleural irritation, which can aid in determining the etiology of the effusion, since most transudative effusions do not cause direct pleural irritation. Its presence raises the likelihood of an exudative etiology such as pleural infection, mesothelioma, or pulmonary infarction. o Pain may be mild or severe. It is typically described as sharp or stabbing and is exacerbated with deep inspiration. o Pain may be localized to the chest wall or referred to the ipsilateral shoulder or upper abdomen, usually because of diaphragmatic involvement. o Pain often diminishes in intensity as the pleural effusion increases in size. y Other symptoms occurring with pleural effusions are associated with the underlying disease process. o Increasing lower extremity edema, orthopnea, and paroxysmal nocturnal dyspnea may all occur with congestive heart failure. o Night sweats, fever, hemoptysis, and weight loss should suggest tuberculosis (TB). o Hemoptysis also raises the possibility of malignancy, other endotracheal or endobronchial pathology, or pulmonary infarction. o An acute febrile episode, purulent sputum production, and pleuritic chest pain may occur in patients with an effusion associated with pneumonia. 

Pathophysiology
Pleural effusion is an indicator of an underlying disease process that may be pulmonary or nonpulmonary in origin, acute or chronic. y Normal pleural fluid has the following characteristics: o Clear ultrafiltrate of plasma that originates from the parietal pleura o pH 7.60-7.64 o Protein content less than 2% (1-2 g/dL) o Fewer than 1000 WBCs per cubic millimeter o Glucose content similar to that of plasma o Lactate dehydrogenase (LDH) less than 50% of plasma

Sodium, potassium, and calcium concentration similar to that of the interstitial fluid y The following mechanisms play a role in the formation of pleural effusion: o Altered permeability of the pleural membranes (eg, inflammation, malignancy, pulmonary embolus) o Reduction in intravascular oncotic pressure (eg, hypoalbuminemia, cirrhosis) o Increased capillary permeability or vascular disruption (eg, trauma, malignancy, inflammation, infection, pulmonary infarction, drug hypersensitivity, uremia, pancreatitis) o Increased capillary hydrostatic pressure in the systemic and/or pulmonary circulation (eg, congestive heart failure, superior vena cava syndrome) o Reduction of pressure in the pleural space, preventing full lung expansion (eg, extensive atelectasis, mesothelioma) o Decreased lymphatic drainage or complete blockage, including thoracic duct obstruction or rupture (eg, malignancy, trauma) o Increased peritoneal fluid, with migration across the diaphragm via the lymphatics or structural defect (eg, cirrhosis, peritoneal dialysis) o Movement of fluid from pulmonary edema across the visceral pleura o Persistent increase in pleural fluid oncotic pressure from an existing pleural effusion, causing further fluid accumulation The net result of effusion formation is a flattening or inversion of the diaphragm, mechanical dissociation of the visceral and parietal pleura, and a restrictive ventilatory defect.
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Medical Management
The free end of the Chest Drainage Device is usually attached to an underwater seal, below the level of the chest. This allows the air or fluid to escape from the pleural space, and prevents anything returning to the chest. Treatment depends on the underlying cause of the pleural effusion. Therapeutic aspiration may be sufficient; larger effusions may require insertion of an intercostal drain (either pigtail or surgical). When managing these chest tubes it is important to make sure the chest tubes do not become occluded or clogged. A clogged chest tube in the setting of continued production of fluid will result in residual fluid left behind when the chest tube is removed. This fluid can lead to complications such as hypoxia due to lung collapse from the fluid, or fibrothorax, late, when the space scars down. Repeated effusions may require chemical (talc, bleomycin, tetracycline/doxycycline) or surgical pleurodesis, in which the two pleural surfaces are scarred to each other so that no fluid can accumulate between them. This is a surgical procedure that involves inserting a chest tube, then either mechanically abrading the pleura, or inserting the chemicals to induce a scar. This requires the chest tube to stay in until the fluid drainage stops. This can be days to weeks and can require prolonged hospitilizations. If the chest tube becomes clogged fluid will be left behind and the pleurodesis will fail.

Pleurodesis fails in as many as 30% of cases. Other treatments for malignant pleural effusions include surgical pleurectomy, insertion of a small catheter attached to the drainage bottle for outpatient management (Pleurex catheter), or implantation of a pleuroperitoneal shunt which consists of two catheters connected by a pump chamber containing two-one way valves. Fluids moves from the pleural space to the pump chamber and then to the peritoneal cavity. The patient manually pumps on the reservoir daily to move fluid from the pleural space to the peritoneal space. Once a pleural effusion is diagnosed, the cause must be determined. Pleural fluid is drawn out of the pleural space in a process called thoracentesis. A needle is inserted through the back of the chest wall in the sixth, seventh or eighth intercostal space on the midaxillary line, into the pleural space. The fluid may then be evaluated for the following: 1. Chemical composition including protein, lactate dehydrogenase (LDH), albumin, amylase, pH and glucose 2. Gram stain and culture to identify possible bacterial infections 3. Cell count and differential 4. Cytopathology to identify cancer cells, but may also identify some infective organisms 5. Other tests as suggested by the clinical situation - lipids, fungal culture, viral culture, specific immunoglobulins 

Nursing Management
Implementing Medical Regimen:  Prepares and positions the patient for thoracentesis  Offers support all throughout the procedure  Record and send thoracentesis fluid amount to laboratory for testing  Monitoring the system s function of chest tube drainage and water seal drainage and recording the amount drainage at prescribed intervals.  If the patient is to be managed as an outpatient with a pleural catheter for drainage, the nurse is responsible for educating the patient and the family regarding management and care of the catheter and drainage system

II.

Cardiac Tamponade

Cardiac tamponade also known as pericardial tamponade, is an emergency condition in which fluid accumulates in the pericardium (the sac in which the heart is enclosed). If the fluid significantly elevates the pressure on the heart it will prevent the heart's ventricles from filling properly. This in turn leads to a low stroke volume. The end result is ineffective pumping of blood, shock, and often death. Cardiac tamponade occurs when the pericardial space fills up with fluid faster than the pericardial sac can stretch. If the amount of fluid increases slowly (such as in hypothyroidism) the pericardial sac can expand to contain a liter or more of fluid prior to tamponade occurring. If the fluid occurs rapidly (as may occur after trauma or myocardial rupture) as little as 100 ml can cause tamponade. 

Diagnosis
Initial diagnosis can be challenging, as there are a number of differential diagnoses, including tension pneumothorax, and acute heart failure. In a trauma patient presenting with PEA (pulseless electrical activity) in the absence of hypovolemia and tension pneumothorax, the most likely diagnosis is cardiac tamponade. Classical cardiac tamponade presents three signs, known as Beck's triad. Hypotension occurs because of decreased stroke volume, jugular-venous distension due to impaired venous return to the heart, and muffled heart sounds due to fluid inside the pericardium. Other signs of tamponade include pulsus paradoxus (a drop of at least 10mmHg in arterial blood pressure on inspiration), and ST segment changes on the electrocardiogram, which may also show low voltage QRS complexes, as well as general signs & symptoms of shock (such as tachycardia, breathlessness and decreasing level of consciousness). Tamponade can often be diagnosed radiographically, if time allows. Echocardiography, which is the diagnostic test of choice**, often demonstrates an enlarged pericardium or collapsed ventricles, and a chest x-ray of a large cardiac tamponade will show a large, globular heart. 

Causes
Tamponade can occur as a result of any type of pericarditis. y HIV infection y Infection - Viral, bacterial (tuberculosis), fungal y Drugs - Hydralazine, procainamide, isoniazid, minoxidil y Postcoronary intervention (ie, coronary dissection and perforation) y Trauma to the chest y Cardiovascular surgery (postoperative pericarditis) y Postmyocardial infarction (free wall ventricular rupture, Dressler syndrome) y Connective tissue diseases -Systemic lupus erythematosus, rheumatoid arthritis, dermatomyositis y Radiation therapy to the chest y Iatrogenic After sternal biopsy, transvenous pacemaker lead implantation, pericardiocentesis, or central line insertion y Uremia y Anticoagulation treatment y Idiopathic pericarditis y Complication of surgery at the esophagogastric junction such as antireflux surgery y Pneumopericardium (due to mechanical ventilation or gastropericardial fistula) y Other causes include hypothyroidism, acupuncture, Still disease, and Duchenne muscular dystrophy y Type A aortic dissection

Other Problems to Be Considered Large pleural effusion: Cases of cardiac tamponade have been reported with large pleural effusions. The increased intrapleural pressure resulting from large pleural effusions can be transmitted to the pericardial space and impair ventricular filling, thus simulating the hemodynamic equivalent of cardiac tamponade. Tension pneumopericardium: The hemodynamic changes simulate acute cardiac tamponade. Clinically, distant heart sounds, bradycardia, and shifting tympany occur over the precordium and a characteristic murmur is heard, termed bruit de la roue de moulin. This is usually observed in infants with mechanical ventilation but is also observed after sternal bone marrow aspiration, penetrating chest wall injury, esophageal rupture, and bronchopericardial fistula. Rapid and labored breathing: Large decreases in intrathoracic pressure with deep inspirations, often observed during respiratory failure, can accentuate the pulsus paradoxus, simulating pericardial tamponade. 

Signs and Symptoms
In a retrospective study, the most common symptoms noted by Roy et al are dyspnea, tachycardia, and elevated jugular venous pressure. Evidence of chest wall injury may be present in trauma patients. Tachycardia, tachypnea, and hepatomegaly are observed in more than 50% of patients with cardiac tamponade, and diminished heart sounds and a pericardial friction rub are present in approximately one third of patients. Some patients may present with dizziness, drowsiness, or palpitations. Cold, clammy skin and weak pulse due to hypotension are also observed in patients with tamponade. y The Beck triad or acute compression triad o Described in 1935, this complex of physical findings refers to increased jugular venous pressure, hypotension, and diminished heart sounds. o These findings result from a rapid accumulation of pericardial fluid. However, this classic triad is usually observed in patients with acute cardiac tamponade. y Pulsus paradoxus or paradoxical pulse o This is an exaggeration (>12 mm Hg or 9%) of the normal inspiratory decrease in systemic blood pressure. o To measure the pulsus paradoxus, patients are often placed in a semirecumbent position; respirations should be normal. The blood pressure cuff is inflated to at least 20 mm Hg above the systolic pressure and slowly deflated until the first Korotkoff sounds are heard only during expiration. At this pressure reading, if the cuff is not further deflated and a pulsus paradoxus is present, the first Korotkoff sound is not audible during inspiration. As the cuff is further deflated, the point at which the first Korotkoff sound is audible during both inspiration and expiration is recorded. If the difference between the first and second measurement is greater than 12 mm Hg, an abnormal pulsus paradoxus is present. o The paradox is that while listening to the heart sounds during inspiration, the pulse weakens or may not be palpated with certain heartbeats, while S1 is heard with all heartbeats.

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A pulsus paradoxus can be observed in patients with other conditions, such as constrictive pericarditis, severe obstructive pulmonary disease, restrictive cardiomyopathy, pulmonary embolism, rapid and labored breathing, and right ventricular infarction with shock. o A pulsus paradoxus may be absent in patients with markedly elevated LV diastolic pressures, atrial septal defect, pulmonary hypertension, and aortic regurgitation. Kussmaul sign o This was described by Adolph Kussmaul as a paradoxical increase in venous distention and pressure during inspiration. o This sign is usually observed in patients with constrictive pericarditis but occasionally is observed in patients with effusive-constrictive pericarditis and cardiac tamponade. Ewart sign o Also known as the Pins sign, this is observed in patients with large pericardial effusions. o It is described as an area of dullness, with bronchial breath sounds and bronchophony below the angle of the left scapula. The y descent o The y descent is abolished in the jugular venous or right atrial waveform. o This is due to an increase in intrapericardial pressure, preventing diastolic filling of the ventricles. Dysphoria: Behavioral traits such as restless body movements, unusual facial expressions, restlessness, sense of impending death were reported by Ikematsu in about 26% patients with cardiac tamponade.5 Low-pressure tamponade: In severely hypovolemic patients, classical physical findings such as tachycardia, pulsus paradoxus, and jugular venous distension were infrequent. Sagrista-Sauleda et al identified low-pressure tamponade in 20% of patients with cardiac tamponade. They also reported low-pressure tamponade in 10% of large pericardial effusions.
o 

Pathophysiology
The pericardium, which is the membrane surrounding the heart, is composed of 2 layers. The thicker parietal pericardium is the outer fibrous layer; the thinner visceral pericardium is the inner serous layer. The pericardial space normally contains 20-50 mL of fluid. Pericardial effusions can be serous, serosanguineous, hemorrhagic, or chylous. Reddy et al describe 3 phases of hemodynamic changes in tamponade. y Phase I: The accumulation of pericardial fluid causes increased stiffness of the ventricle, requiring a higher filling pressure. During this phase, the left and right ventricular filling pressures are higher than the intrapericardial pressure. y Phase II: With further fluid accumulation, the pericardial pressure increases above the ventricular filling pressure, resulting in reduced cardiac output. y Phase III: A further decrease in cardiac output occurs, which is due to equilibration of pericardial and left ventricular (LV) filling pressures.

The underlying pathophysiologic process for the development of tamponade is markedly diminished diastolic filling because transmural distending pressures are insufficient to overcome the increased intrapericardial pressures. Tachycardia is the initial cardiac response to these changes to maintain the cardiac output. Systemic venous return is also altered during tamponade. Because the heart is compressed throughout the cardiac cycle due to the increased intrapericardial pressure, systemic venous return is impaired and right atrial and right ventricular collapse occurs. Because the pulmonary vascular bed is a vast and compliant circuit, blood preferentially accumulates in the venous circulation, at the expense of LV filling. This results in reduced cardiac output and venous return. The amount of pericardial fluid needed to impair the diastolic filling of the heart depends on the rate of fluid accumulation and the compliance of the pericardium. Rapid accumulation of as little as 150 mL of fluid can result in a marked increase in pericardial pressure and can severely impede cardiac output2 , whereas 1000 mL of fluid may accumulate over a longer period without any significant effect on diastolic filling of the heart. This is due to adaptive stretching of the pericardium over time. A more compliant pericardium can allow considerable fluid accumulation over a longer period without hemodynamic insult. 

Management
Cardiac tamponade is a medical emergency. Preferably, patients should be monitored in an intensive care unit. y All patients should receive the following: o Oxygen o Volume expansion with blood, plasma, dextran, or isotonic sodium chloride solution, as necessary to maintain adequate intravascular volume. o Bed rest with leg elevation: This may help increase venous return. o Inotropic drugs (eg, dobutamine): These can be useful because they do not increase systemic vascular resistance while increasing cardiac output. y Positive-pressure mechanical ventilation should be avoided because it may decrease venous return and aggravate signs and symptoms of tamponade. y Further medical care includes pericardiocentesis. Removal of pericardial fluid is the definitive therapy for tamponade and can be done by the following 3 methods. o Emergency subxiphoid percutaneous drainage: This is a life-saving bedside procedure. The subxiphoid approach is extrapleural; hence, it is the safest for blind pericardiocentesis. A 16- or 18-gauge needle is inserted at an angle of 3045° to the skin, near the left xiphocostal angle, aiming towards the left shoulder. When performed emergently, this procedure is associated with a reported mortality rate of approximately 4% and a complication rate of 17%. o Echocardiographically guided pericardiocentesis (often performed in the cardiac catheterization laboratory): This is usually performed from the left intercostal space. First, mark the site of entry based on the area of maximal fluid accumulation closest to the transducer. Then, measure the distance from the skin to the pericardial space. The angle of the transducer should be the

y

trajectory of the needle during the procedure. Avoid the inferior rib margin while advancing the needle to prevent neurovascular injury. Leave a 16-gauge catheter in place for continuous drainage. o Percutaneous balloon pericardiotomy: This can be performed using an approach similar to that for echo-guided pericardiocentesis, in which the balloon is used to create a pericardial window. Patients should receive treatment of the underlying cause to prevent recurrence.

Surgical Care For a hemodynamically unstable patient or one with recurrent tamponade, provide the following care: y Surgical creation of a pericardial window: This involves the surgical opening of a communication between the pericardial space and the intrapleural space. This is usually a subxiphoidian approach with resection of xiphoid. Recently, a left paraxiphoidian approach with preservation of xiphoid has been described.Open thoracotomy and/or pericardiotomy3 may be required in some cases, and these should be performed by an experienced surgeon. y Pericardiocentesis or sclerosing the pericardium: This is a therapeutic option for patients with recurrent pericardial effusion or tamponade. Through the intrapericardial catheter, corticosteroids, tetracycline, or antineoplastic drugs (eg, anthracyclines, bleomycin) can be instilled into the pericardial space. y Pericardio-peritoneal shunt: In some patients with malignant pericardial effusions, creation of a pericardio-peritoneal shunt helps prevent recurrent tamponade. y Pericardiectomy: Resection of the pericardium (pericardiectomy) through a median sternotomy or left thoracotomy is rarely required to prevent recurrent pericardial effusion and tamponade. Medication The role of medication therapy in cardiac tamponade is limited. Occasionally, inotropic agents that do not increase the peripheral vascular resistance, such as dobutamine, may be used. Adrenergic agonist agents By stimulating beta-1 receptors in the heart, stroke volume and cardiac output are increased. Dobutamine (Dobutrex) Synthetic catecholamine and a direct inotropic agent that stimulates cardiac betareceptors with minimal increase in systemic vascular resistance.

LICEO DE CAGAYAN UNIVERSITY COLLEGE OF NURSING N103 TEACHING LEARNING GUIDE Topic Level of student Venue C.I. : Pleural Effusion and Cardiac Tamponade : N103- Section A, Group C2 : Liceo de Cagayan University Campus, HB Room : Mrs. Gina Batasin-in, RN, MN

SCORE: ________

Date and Time : September 15, 2010 Reporter : Torregosa, Cyrus Dan A., SN

General Objective: At the end of 35 minutes, I will be able to present and discuss effectively the disease topic about Pleural Effusion and Cardiac Tamponade assigned to me, as well as, the students will gain and increase knowledge from the discussion.

Specific Objective

Content

Time Allotment

Teaching Learning Activities Teacher Student

Evaluation

Reference Books: ³Textbook of MedicalSurgical Nursing´, 11th Edition, Volume I, pp.652-654, 680´.Lippincott Wiliams and Wilkins 2008. Internet Sources:  http://en.wikipedia.org/ wiki/pleuraleffusion  http://en.wikipedia.org/ wiki/Cardiac_tampona de  http://emedicine.medsc ape.com/article/15208

At the end of 35 minutes, the students will be able to: a. Acquire new knowledge about Pleural Effusion and Cardiac Tamponade and verbalize the understanding about it b. Know the causes, signs and symptoms, treatment and management of the disease.

Brief discussion of the Pleural Effusion and Cardiac Tamponade assigned to me: y y y y y Definition Causes/Risk Factors Signs and Symptoms Diagnostic Exams Treatment and Management 35 min

Ask questions and give further information regarding the topic.

Active listening and participation. Ask questions.

Quiz (Post- Test)

LICEO DE CAGAYAN UNIVERSITY COLLEGE OF NURSING N103 TEACHING LEARNING GUIDE Topic Level of student Venue C.I. : The Surgical Experience : N103- Section A, Group C2 : Liceo de Cagayan University Campus, HB Room : Mr. Roberto Alli III, RN, MN

SCORE: ________

Date and Time : September 09, 2010 Reporter : Torregosa, Cyrus Dan A., SN

General Objective: At the end of 25 minutes, I will be able to present and discuss effectively the topic about the Intra-operative Nursing Management specifically the Surgical Experience assigned to me, as well as, the students will gain and increase knowledge from the discussion.

Specific Objective

Content

Time Allotment

Teaching Learning Activities Teacher Student

Evaluation

Reference

At the end of 25 minutes, the students will be able to: c. Acquire new knowledge about the Intraoperative Nursing Management: Surgical Experience and verbalize the understanding about it

Brief discussion of the expanded Intra-operative Nursing Management: Surgical Experience assigned to me: -Types of Anesthesia and Sedation y General Anesthesia y Regional Anesthesia y Moderate Sedation y Monitored Anesthesia Care y Local Anesthesia

Books: Ask questions and give further information regarding the topic. Active listening and participation. Ask questions. Quiz (Post- Test) ³Textbook of Medical-Surgical th Nursing´, 11 Edition, Volume I, pp.508-516 ´.Lippincott Wiliams and Wilkins 2008. Internet Sources: http://en.wikipedia.org/wiki/Ane sthetic

25 min

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