Thierry H. LeJemtel, MD

• Department of Medicine
• Division of Cardiology
• Tulane University School of Medicine
• New Orleans, LA

If the radius of the tube is halved antifungal talcum powder buy butenafine 15 mg without prescription, the pressure required to maintain a given flow rate must be increased 16 times antifungal groin cream 15 mg butenafine purchase amex. The airflow is no longer directly proportional to the driving pressure as with laminar flow; rather fungus forest best 15 mg butenafine, the driving pressure to produce a given rate of airflow is proportional to the square of flow (P V 2) antifungal pet shampoo order 15 mg butenafine with amex. Also fungus kills ants order butenafine, the driving pressure is dependent on gas density but is little affected by viscosity. Turbulent flow dominates in the more central airways, where V is high because airway caliber is large but the total cross-section area is small. It is apparent that turbulence is most likely to occur when the rate of airflow and the gas density are high, the viscosity is low, and the tube radius is small. With a mixed flow pattern, the driving pressure to produce a given flow depends on both the viscosity and the density of the gas. In addition to pressure dissipation to generate flow, expiration requires some energy to accelerate the gas moving from the large cross-sectional area of the respiratory zone to the smaller cross-sectional area of conducting zone (bronchi, trachea). The P caused by convective acceleration is described by the Bernoulli 2 equation, P = 1 2 (V A), where A is cross-section area. In the remainder of the tracheobronchial tree, flow is transitional, and in the trachea, turbulence regularly occurs. As lung volume decreases, its recoil pressure decreases, the intrathoracic airways narrow, the airway resistance increases, and the airflow decreases almost linearly. At all lung volumes, pleural pressure becomes less subatmospheric and subsequently exceeds atmospheric pressure as the expiratory effort is progressively increased. Because airflow remains constant despite an increase in driving pressure, it follows that the resistance to airflow must also be increasing proportionally with pleural pressure, Central airways have a small total cross-sectional area and account for approximately 90% of airway resistance Peripheral airways (2 mm diameter) contribute only about 10% of total airway resistance of normal lung because the number of airways and total cross-sectional area in any generation are very large probably because of compression and narrowing of intrathoracic airways. Because airflow has ceased, pressures along the entire airway are also at atmospheric levels. During a forced expiration, pleural pressure increases above atmospheric pressure and increases alveolar pressure. Airway pressure decreases progressively from the alveolus toward the airway opening to overcome viscous resistance. As soon as maximal expiratory flow is achieved, further increases in pleural pressure with increasing expiratory force simply produce more compression of the downstream segment but do not affect airflow through the upstream segment. This is because a maximal effort is not required to achieve maximal flow at intermediate and low lung volumes. Thus, parameters measured over most of a forced expiratory maneuver are little affected by suboptimal efforts and are good, albeit indirect, indexes of airway resistance. Comparing tidal with forced expiratory flow-volume curves allows one to estimate the occurrence of expiratory flow limitation during breathing. Driving pressure is proportional to square of flow and is dependent on gas density Transitional flow occurs in larger airways, particularly at branches and at sites of narrowing. When maximal flow is attained during tidal breathing because of bronchoconstriction or exercise hyperpnea, the only way to maintain or increase minute ventilation is to breathe at increased lung volume, at which greater expiratory flows can be generated. Flow limitation during tidal expiration may be present either in obstructive disorders because maximal flows are reduced or in restrictive disorders because breathing occurs at low lung volume. In restrictive disorders, all lung volumes are reduced, and flow is low throughout expiration even if, with respect to absolute lung volume, it may be greater than normal. Dynamic Lung Compliance and Work of Breathing (see Plate 2-12) Changes in lung volume and pleural pressure during a breathing cycle, displayed as a pressure-volume loop, describe elastic and flow-resistive properties of the lung as well as the work performed by the respiratory muscles on the lung. The slope of the line connecting endexpiratory and end-inspiratory points on the pressurevolume loop provides a measure of dynamic lung compliance. In addition, during inspiration, the change in pleural pressure at any given lung volume reflects not only the pressure needed to overcome lung elastic recoil but also the pressure required to overcome airway and lung tissue resistances. Alveolar pressure (sum of pleural pressure and lung recoil pressure) is yet higher (+30 cm H2O). Fall in airway pressure and location of equal pressure point are unchanged, but beyond equal pressure point, intrathoracic airways will be compressed to a greater degree by higher pleural pressure. For the distribution of ventilation to parallel lung units to be independent of airflow, their time constants. The mechanical work of breathing (W) performed by the respiratory muscles can be readily evaluated during spontaneous breathing from changes in pleural pressure (P) and lung volume (V) according to the equation: W = PdV During quiet breathing, lung elastic recoil is sufficient to overcome nonelastic forces during expiration, which is therefore passive. From the point of view of energy requirements, the work of breathing can be considered as oxygen cost of breathing. In normal individuals, this is approximately 1 mL oxygen per liter of ventilation, which is less than 5% of total oxygen consumption but increases with increasing ventilation. Thus, the oxygen consumed by respiratory muscles can be inferred from the increase in total oxygen consumption when ventilation is increased, either voluntarily or in response to breathing carbon dioxide. Because of these differences in pleural pressure, the transpulmonary pressure is greater at the top than at the bottom of the lung, so at most lung volumes, the alveoli at the lung apices are more expanded than those at the lung bases. The distribution of ventilation and volume at which airways at the lung bases begin to close can be assessed by the single-breath nitrogen washout and closing volume test (see Plate 2-13). The initial portion of the inspiration, which consists of dead-space gas rich in nitrogen, goes to the upper lung zones, and the remainder of the breath, containing only oxygen, is distributed preferentially to the lower lung zones. During the subsequent expiration, the initial portion of the washout consists of dead space and contains no nitrogen (phase I). Then, as alveolar gas containing nitrogen begins to be washed out, the concentration of nitrogen in the expired air rises to reach a plateau. At low lung volumes, when the airways at the lung bases close, only the alveoli at the top of the lung continue to empty. The volume at which this increase in slope occurs is referred to as the closing volume. Contraction of the right ventricle delivers the entire cardiac output along the pulmonary arteries to the capillary bed where gas exchange takes place. The pulmonary capillaries consist of a fine network of thin-walled vessels, but because the surface area of the capillary bed is approximately 70 m2, it may be regarded as a sheet of flowing blood rather than as individual channels. At any one moment, the pulmonary capillary bed holds only about 100 mL of blood; most of the remainder of the blood in the pulmonary circulation is contained in the compliant pulmonary venules and veins which, along with the left atrium, serve as a reservoir for the left ventricle. Intravascular Pressure the systemic circulation distributes blood flow to various organs such as the muscles, kidneys, and gastrointestinal tract in response to their specific requirements. By contrast, the pulmonary circulation is concerned only with blood flow through the lungs. Pulmonary vascular pressures are very low compared with those in the systemic circulation; systolic pulmonary artery pressure is approximately 25 mm Hg, diastolic pressure is 8 mm Hg, and mean arterial pressure is about 14 mm Hg. Pressure in the left atrium is 5 mm Hg, only slightly less than the pressure in the large pulmonary veins. This causes the pattern of blood flow distribution to decrease with distance from the hilum of the lung. Normally, pulmonary artery pressure is just sufficient to deliver blood to the lung apices at rest. Farther down the lung, there is a region called zone 2 within which pulmonary artery pressure is greater than alveolar pressure because of the hydrostatic gradient, but where alveolar pressure is still greater than venous pressure. Still farther down the lung, gravity increases hydrostatic vascular pressures to the point that venous pressure exceeds alveolar pressure. Within this region, known as zone 3, blood flow is determined principally by the difference between pulmonary arterial and venous pressures. It follows that pulmonary vascular resistance is one-tenth of the systemic resistance. The major sites of pulmonary vascular resistance are the arterioles and capillaries. The pulmonary circulation is able to accommodate several fold increases in Qc, such as occur during exercise, with only small changes in pulmonary artery pressure. Pulmonary blood vessels are extremely thin walled and compliant, so their caliber is greatly influenced by transmural pressure. Increases in alveolar pressure produced, for example, by positivepressure mechanical ventilation can compress these vessels to the point of closure. Factors Affecting the Pulmonary Vascular Bed A variety of neural stimuli as well as chemical and humoral substances can affect the pulmonary vascular bed (see Plate 2-15). Hypoxemia, on the other hand, is a potent stimulus that constricts both precapillary and postcapillary vessels. The effects of hypercapnia on the pulmonary vasculature are variable and appear to depend on changes in hydrogen ion concentration. Acidosis, whether respiratory or metabolic, increases pulmonary vascular tone, and acidosis and hypoxemia together are considered to act synergistically in constricting pulmonary vessels and increasing pulmonary vascular resistance. Chemical and humoral agents that produce pulmonary vasoconstriction include epinephrine, norepinephrine, histamine, angiotensin, and endothelin-1. Idiopathic pulmonary arterial hypertension leads to remodeling of pulmonary blood vessels, thickening their walls and decreasing luminal caliber. These disorders cause the heart to have to exert increased forces of contraction to maintain blood flow through the lungs, which can lead eventually to hypertrophy, strain, and ultimately failure of the right ventricle. Pleural pressure in upright position is more subatmospheric at top of lung and increases down lung consequent to weight of lung and force of gravity 40 4 Pleural pressure At low lung volumes, alveoli at top of lung are larger than those at bottom. A single full breath of 100% O2 is inhaled from residual volume to total lung capacity. Remainder of breath (O2 only) preferentially goes to lower lung zones, so concentration N2 is lower in alveoli of lung bases. During subsequent expiration, concentration of N2 at mouth is plotted against expired lung volume Phase I. Thus, for example, in a gas at a pressure of 760 mm Hg (1 atm) in which 80% of the molecules are nitrogen and 20% are oxygen, the partial pressure of nitrogen is 0. Thereafter, inspired gas molecules mix with resident alveolar gas and make their way to the blood-gas barrier largely by diffusion. The distance over which gases have to diffuse to reach the blood-gas barrier is small in normal alveoli, and complete mixing of newly inspired air with resident gas occurs within a fraction of a second. By contrast, when the alveolar spaces are enlarged as occurs in emphysema, the diffusive transport time may be prolonged to the point of becoming a limiting factor in gas transfer. Membrane Diffusion Gas transfer across the alveolar-capillary membrane involves diffusion between gas and liquid phases, as well as diffusion within the liquid phase. The rates at which these processes occur depends on the solubility of the gas in the liquid. Barriers to Diffusion There are a sequence of barriers that oxygen and carbon dioxide must cross to move between alveolus and blood. These are collectively known as the blood-gas barrier and include the fluid layer that lines the alveoli, the alveolar epithelium and its underlying basement membrane, a region of interstitial fluid, the capillary endothelium, a layer of plasma in the capillary blood, and the red blood cell membrane. The difference in the partial pressures of oxygen (Po2) between alveolar air and pulmonary capillary blood is greatest at the beginning of the capillary where venous blood enters with a Po2 of about 40 mm Hg. Oxygen moves down its concentration gradient from alveolus to capillary blood, causing the Po2 of the blood to increase as it moves past the blood-gas barrier. The alveolar Po2 does not fall at the same rate because the combined oxygen storage capacity of the alveoli is much greater than that of the blood adjacent to the blood-gas barrier. However, in normal lungs, the diffusion of oxygen across the bloodgas barrier is so rapid that the Po2 of the blood reaches that of the alveolar air before the blood has passed even halfway along the alveolar capillaries. Certain diseases, however, may compromise the diffusive capacity of the blood-gas barrier, either by thickening it such as occurs in pulmonary edema and fibrosis or by decreasing its total area as occurs in emphysema. Alveolar pressure exceeds arterial pressure, and there is no blood flow to this area. Arterial pressure exceeds alveolar pressure, and alveolar pressure exceeds venous pressure. Blood flow depends on arterial-venous pressure difference, which is constant throughout the zone. Because arterial pressure increases down zone, transmural pressure becomes greater, capillaries distend, and resistance to flow falls the diffusion rate of carbon dioxide across the blood-gas barrier greatly exceeds that of oxygen, so the time required for equilibrium between alveolar air and capillary blood is correspondingly less. Thus, even when diffusion is considerably impaired, the alveolararterial partial pressure gradient for carbon dioxide remains small. Diffusing Capacity and Its Components the diffusing capacity of the lung is a measure of the ease with which a gas is able to move from the alveoli to the capillary blood and is defined as the flow of gas normalized to its mean partial pressure gradient across the blood-gas barrier. This means that the diffusing capacity for these gases only becomes a rate-limited step in gas transport in cases of extreme pathology, such as severe emphysema or pulmonary edema. Thus, neither oxygen nor carbon dioxide is limited by its rates of diffusion across the blood-gas barrier and so cannot be used to measure the diffusing capacity of the lungs. This property is what makes carbon monoxide so dangerous, but here it can be used to advantage. Effects of increases in pulmonary blood flow and vascular pressures Arteriole Capillaries Normally, some pulmonary capillaries are closed and conduct no blood Recruitment: More capillaries open as pulmonary vascular pressure or blood flow increases Distension: At high vascular pressures, individual capillaries widen and acquire a larger crosssectional area B. The membrane component of diffusion resistance increases when the alveolar walls are damaged (emphysema) or when pulmonary blood flow is obstructed (pulmonary embolism, vascular disease) because these conditions reduce the effective area across which diffusion can occur. Diffusion resistance is also increased by increases in the thickness of the blood-gas barrier. Effective tissue thickening may also occur within the blood portion if the diffusion distance across the plasma increases because of either dilatation of the pulmonary capillaries or scarcity of red blood cells (hemodilution). The remaining approximately 1% of air is comprised of carbon dioxide (<1 mm Hg), water vapor, and inert gases such as argon and neon. Inspired atmospheric air is warmed and humidified as it passes through the nasopharynx and tracheobronchial tree. Normally, mean alveolar Pco2 and Po2 are approximately 100 mm Hg and 40 mm Hg, respectively. Pulmonary capillary blood normally removes oxygen from the lungs at a greater rate than it delivers carbon dioxide to the lungs.

For nasotracheal suction fungus roses discount 15 mg butenafine free shipping, a soft latex or polyvinyl 32- or 34-Fr nasopharyngeal airway antifungal body wash cvs buy butenafine 15 mg amex, lubricated with lidocaine jelly antifungal lip balm cheap 15 mg butenafine with visa, is inserted into the nose and advanced so that its distal tip lies above the vocal cords fungus plant order butenafine cheap online. Introduction of the suction catheter in this way prevents trauma to the nasal mucosa and larynx and minimizes the deposition of upper airway secretions into the lung fungi questions generic 15 mg butenafine mastercard. After passing the vocal cords, the catheter is advanced until it reaches the main bronchi. Because the right mainstem bronchus has a more vertical orientation than the left mainstem bronchus, the catheter more frequently enters the right-sided airways. It also stimulates coughing, which facilitates clearance of secretions from the major bronchi. By minimizing disconnections from the ventilator, inline suctioning avoids derecruitment and reduces the risk of nosocomial infection. Hypoxemia may be minimized by limiting the duration of suctioning to 3 to 5 seconds and administering 100% oxygen for about 1 minute before the procedure. It should be understood that all suction catheters traumatize the tracheobronchial mucosa in two ways: (1) by causing invagination of the mucosa into the end or side holes with consequent immediate ischemic necrosis of the area and (2) by direct physical contact, which results in delayed sloughing of ciliated epithelium many hours later. Mechanical ventilation is continued until the condition responsible for respiratory failure improves and the patient can successfully resume adequate spontaneous respiration. The volume delivered is set by the operator; the resulting pressure is the dependent variable. A ventilator can be set to control the flow applied and volume delivered during inspiration (right side of Eq 2), and the pressure applied by the ventilator is determined by the elastic recoil and resistance properties of the respiratory system. Because flow and volume are so closely related, this is conventionally called volumecontrol ventilation, even though most ventilators actually regulate flow. Alternatively, the ventilator can be set to apply a clinician-set airway pressure for a set time interval (left side of Eq 2). The blue line shows the square wave of airway pressure (Paw) applied during inspiration, generated by the decelerating flow pattern shown in purple. Complications After a patient has been placed on mechanical ventilation, the clinician must try to minimize the associated complications. Because the rate of complications from mechanical ventilation increase with time, it is important to evaluate patients for liberation from mechanical ventilation on a daily basis. If only anterior and lateral walls of trachea are involved in stenosis, those portions are excised. If more extensive excision is required, approximation may not be readily accomplished without undue tension on suture line, and measures to bring ends of trachea together become necessary D. Common areas of stenosis were previously located in the mid-trachea related to high-pressure, low-volume endotracheal tube cuffs; however, contemporary endotracheal appliances have low-pressure cuffs. Today stenotic lesions are typically found in the proximal or subglottic trachea at the site of a prior stoma. The procedure of choice is resection of the stenotic tracheal segment with primary reconstruction via an end-to-end anastomosis (see illustration). Resection and primary reconstruction are more easily accomplished if the lesion is in the cervical portion of the trachea than if it is within the mediastinum. Nevertheless, the lumen must be examined via a transverse incision at the lower end of the constriction to determine whether the stenosis is circumferential or confined to the anterior and lateral cartilaginous walls of the trachea. If upper tracheal relaxation is necessary, the larynx can be "dropped" by a suprahyoid release (dotted line), which involves cutting the muscles above the hyoid bone or an inferior hyoid release achieved by cutting the thyrohyoid muscle, thyrohyoid membrane, and upper fibers of the inferior constrictor, with care taken to avoid injury to the superior laryngeal artery and nerve H. Low intrathoracic airway lesions may be approached via a high (4th interspace) right posterolateral thoracotomy. For extensive proximal tracheal resections, a suprahyoid or infrahyoid release may facilitate approximation of the divided tracheal ends. To relieve tension on an intrathoracic reconstruction, these cervical maneuvers provide minimal additional length. Releasing one or both inferior pulmonary ligaments as well as incision of the right-sided pericardial attachments to the atrium and inferior pulmonary vein is more efficacious. If the chest, on lateral view, is divided into three roughly equal compartments in an anteroposterior plane, the most common tumors are as follows: (1) anterior/superior mediastinum-thymoma, germ cell tumors (mature teratoma, teratocarcinoma, yolk sac tumor), lymphoma, and intrathoracic thyroid extension (including substernal thyroid); (2) middle/visceral mediastinum- congenital bronchopulmonary foregut cysts and tumors of lymphoid involvement (Hodgkin and non-Hodgkin lymphomas and metastatic cancer); and (3) posterior mediastinum-tumors of neurogenic origin (neurofibroma) and esophageal lesions. Patients presenting with symptoms (localized or generalized) have a malignant process 85% of the time. The illustration shows removal of a neurofibroma, the most common mediastinal tumor, which, characteristically, hugs the posterior costovertebral angle. The presence of an intraspinal component ("dumbbell" tumor) should be ruled out preoperatively by means of magnetic resonance imaging of the spine showing the intervertebral foramina. When the tumor is large or densely adherent, this approach may present difficulties because the tumor lies between the operator and the vital structures from which it must be freed. Recent evidence suggests anatomic segmentectomy may provide survival equivalent to lobectomy for small (2 cm) primary lung cancers in the absence of regional node involvement. Segmentectomy requires a detailed anatomic knowledge of secondary and tertiary hilar structures. Intersegmental cleavage planes are best defined at operation when, by selective bronchial occlusion, adjacent portions of lung tissue are maintained, one inflated and the other atelectatic. The segmental artery or arteries are located, carefully dissected free, and divided after appropriate proximal and distal ligation. The segmental bronchus is closely adjacent and then may be palpated and dissected free. To ensure correct identification of the proper bronchus after it is dissected free, one carries out temporary atraumatic occlusion of this structure while the remainder of the lobe is being inflated by the anesthesiologist. Separation of the intersegmental plane is performed either with a stapling device, which simultaneously controls the veins and parenchyma, or by blunt dissection with the fingers, working toward the pleural surface Left pulmonary artery Aorta Segmental artery doubly ligated and divided Wedge resection or open lung biopsy Using stapling-cutting device while exercising traction on the clamp attached to the distal divided bronchus. Venous branches on the segmental surface are grasped by small hemostats before cutting and subsequently ligated with fine suture material. These veins can serve as a helpful guide to the intersegmental plane as dissection proceeds. Less lung tissue is removed, as a rule, than with segmental resection, and the procedure is simpler, safer, and quicker. Pulmonary vein branches pass between bronchopulmonary segments and lobes, but pulmonary arterial branches generally follow the bronchial tree. An incomplete fissure may be congenital or the result of inflammation or a pathologic process extending across the fissure. Separating the lobes often requires sharp and blunt dissection and may require the use of a mechanical stapling device. The key to anatomic pulmonary surgery is a detailed understanding of bronchopulmonary anatomy with careful dissection directly on the branch pulmonary arteries. After proximal ligation has been accomplished, it is usually possible to dissect distally along the branch so that placement of the distal tie will permit leaving a long proximal stump when the branch artery is divided. Often segmental branch arteries have a common trunk, which can be ligated proximally while distal control is obtained of each segmental vessel. The main artery is followed down the oblique fissure, exposing its anterior and posterior aspects. The lowermost branches to the upper lobe supply the lingula and come off anteriorly. Directly opposite, on the posterior aspect of the continuing left main pulmonary artery, the artery to the superior segment of the lower lobe takes origin, and this should be carefully preserved. The lung is then retracted posteriorly for dissection of the superior pulmonary vein, which drains the upper lobe, including the lingula on the left side. An atraumatic bronchial clamp or noncutting stapler is then placed across the bronchus, and the anesthesiologist is asked to inflate the lung. Correct identification of the bronchus clamped is ensured when the lower lobe inflates and the upper remains collapsed. Anterior and apical-posterior segmental arteries ligated, suture ligated, and divided Lingular artery Anterior segmental artery Apicalposterior segmental artery Basal arteries Superior segmental artery of lower lobe B. Segmental arteries successively ligated and divided from above downward with care to preserve superior segmental artery of lower lobe C. The stapling device is then fired across the bronchus close to its origin and the bronchus is amputated on the distal aspect of the anvil after stapling. The main pulmonary artery is exposed as it emerges from beneath the arch of the aorta, and care is exercised to avoid the left recurrent nerve as it passes beneath the aortic arch. The arterial branches of the left main pulmonary artery may number five or more, and there are considerable variations in their location. Thus, if an arterial tear or hemorrhage occurs later on, it becomes a simple matter to place a vascular clamp or tourniquet across the vessel and gain control. When an upper lobe lobectomy is performed for cancer, the mediastinum should be opened and all lymph nodes cleared to the carina (or beyond) if suspicion of lymphatic metastasis exists. The procedure was carried out for bronchogenic carcinoma in a fellow physician, James Gilmore, who eventually outlived his surgeon. The technique of pneumonectomy has been improved and standardized in the intervening years, and the results are quite gratifying when the operation is carefully performed in appropriately selected cases. A curved incision is made, starting midway between the vertebral border of the scapula and the spine, clearing the angle of the scapula by one to two fingerbreadths and continuing forward in a transverse direction following the angle of the ribs to a submammary position. The standard incision involves division of the entire latissimus dorsi muscle, but the serratus anterior muscle can often be separated from its posterior border and detached from anterior rib Superior pulmonary vein Azygos vein B. Right pulmonary artery ligated proximally and distally with suture-ligature applied to artery prior to its division (broken line) Right pulmonary artery insertions, preserving its function. With exposure of the subscapular space, the ribs are counted from the first rib downward. Entry through the fifth intercostal space along the superior border of the sixth rib is the standard approach to both pneumonectomy and any lobectomy. After the lesion has been determined to be resectable for cure, hilar dissection is started. The superior pulmonary vein is similarly freed up and divided, exposing the anterior aspect of the right main bronchus. Division of any or all critical hilar structures can be accomplished with suture or mechanical stapling devices. The lung is then retracted superiorly and anteriorly to expose the inferior pulmonary vein along the superior margin of the inferior pulmonary ligament. The right main bronchus is cleared and clamped after lymph nodes and areolar tissue have been swept distally onto the specimen. After driving staples home, bronchus is divided and lung removed of the carina and a stapling device placed across it immediately below its origin. The bronchial stump is then tested under saline for air leakage by having the anesthesiologist apply positive airway pressure (20-25 cm H2O) via the endotracheal tube. The stump should be buttressed with vascularized tissue such as pericardium, intercostal muscle, or parietal pleura. It is useful in the evaluation and management of patients with pleural disease, benign and malignant pulmonary parenchymal neoplasms or diseases, mediastinal masses or adenopathy, and esophageal pathology and for resection of posterior mediastinal neurogenic tumors or conditions responsive to sympathectomy. Most standard thoracic surgical instruments have been modified for thoracoscopic surgery. Preparation for a thoracoscopic operation is similar to that for thoracotomy because the need for conversion to a conventional open surgical approach may arise. An angled videoscope allows superior visualization of the pleural space and central pulmonary vessels and bronchi without interfering with other endoscopic instrumentation. Flexible thoracoscopes allow even greater visualization and are becoming more common. The ports should face the lesion in an approximately 180degree arc placed widely apart to prevent instrument crowding. The hilar structures are individually dissected, and the vessels and bronchi are isolated and controlled. The utility incision can also be enlarged and a lung clamp used to bring lung tissue to the incision for direct digital palpation. If the course continues to be uneventful, the tubes are typically removed on the first postoperative day. Current practice favors stapled bilateral resection over plication or laser ablation to achieve lung volume reduction. When performed through a sternotomy, the resection progresses from an anteromedial orientation and is completed posteriorly and laterally near the tip of the superior segment of the lower lobe. This is the only intervention for emphysema since the availability of portable supplemental oxygen to show a survival benefit. With the exception of a small number of cases of sarcoidosis and lymphangioleiomyomatosis, the original lung disease does not usually recur after lung transplantation. The contralateral lung is not removed, so single-lung transplantation is not performed in patients with bilaterally infected lungs. There has been a trend over the past decade in favor of bilateral transplants for nearly all indications. Heart-lung transplantation was initially the most common type of lung transplant procedure but is now performed infrequently (75 cases in the United States in 2007). Complete separation of epiphysis from shaft through calcified cartilage (growth zone) of growth plate. Intraarticular fracture through epiphysis, across deep zone of growth plate to periphery. Fracture line extends from articular surface through epiphysis, growth plate, and metaphysis. If fractured segment not perfectly realigned with open reduction, osseous bridge across growth plate may occur, resulting in partial growth arrest and joint angulation Type V. Severe crushing force transmitted across epiphysis to portion of growth plate by abduction or adduction stress or axial load.

They may be treated with antibiotics and total parental nutrition fungus in mulch discount butenafine 15 mg on line, and no food may be allowed by mouth for 1 to 2 weeks antifungal yeast treatment buy discount butenafine 15 mg. Another option is endoscopic clipping of a mucosal defect fungus in sinus butenafine 15 mg order on-line, which can be performed with a doublelumen endoscope fungus gnats cider vinegar purchase butenafine 15 mg mastercard. Percutaneous drainage or closure may be performed to treat cervical rupture fungus gnats weed cheap 15 mg butenafine visa, if diagnosed early. If severe soilage occurs, patients should undergo esophagectomy with delayed reconstruction, because they will do better than with drainage alone. For patients with lifethreatening illness, excision of the esophagus is performed. Covered metallic stents may be used to seal perforations in patients with distal esophageal perforation. Large-diameter stents are placed, thoracostomy tubes drain pleural cavities, and antibiotics are administered. Complete sealing occurs in 80% of patients; no further therapy is necessary except for eventual removal of the stent. Treatment is shifting toward the possibility of primary esophageal repair of nonmalignant esophageal perforations that present at any time. Often, however, patients with esophageal injury have an acute attack or "ripping" chest, back, and epigastric pain. Patients with cervical injuries frequently have dysphagia and odynophagia, which increases with neck flexion. Thoracic perforations cause not only substernal chest pain but also epigastric pain. Substernal pain, cervical crepitus, and vomiting affect 60% of patients with spontaneous rupture from barotrauma. Fever, dyspnea, cyanosis, sepsis, shock, and eventually multiorgan failure may develop with increasing contamination of the mediastinum and chest. An hour after the incident, the chest radiograph may show air under the diaphragm or subcutaneous or mediastinal emphysema in 40% of patients. Survival rates are 92% for patients with thoracic perforations closed primarily within 1 day of injury and 30% to 35% for patients with thoracic perforations discovered after 24 hours. In the past, results included 10% to 25% mortality if the perforations were treated within the first 24 hours and 40% to 60% mortality if treated after 48 hours. The mortality rate is highest, 67%, in patients with spontaneous rupture of the esophagus. Zubarik R, Eisen G, Mastropietro C, et al: Prospective analysis of complications 30 days after outpatient upper endoscopy, Am J Gastroenterol 94:15391545, 1999. Floch 20 ties, because surgical treatment may need to be modified if these have developed. A typical finding is a "honeycomb" formation produced by a thin layer of barium surrounding the venous protrusion that does not constrict the lumen. Endoscopic color Doppler ultrasonography is a useful modality for obtaining color flow images of esophageal varices and their hemodynamics. Capsule endoscopy is now being studied as a possible screening tool for esophageal varices; it has a sensitivity and specificity of 84% and 88%, respectively. It also has the benefit of detecting extraluminal pathology that cannot be seen by endoscopy. V aricosities occur secondary to portal hypertension and are defined as a dilatation of various alternative pathways when cirrhosis obstructs the portal return of blood. Varicosities occur most often in the distal third but may occur throughout the esophagus. Varices of the esophagus are a less common cause of upper gastrointestinal hemorrhage, but the consequences of bleeding are an ever-impending threat to life. The most common cause for portal hypertension, affecting 94% of patients, is cirrhosis. The most common causes of cirrhosis are alcoholism (57%), hepatitis C virus (30%), and hepatitis B virus (10%). Mortality rates from the initial episode of variceal hemorrhage range from 17% to 57%. Hospitalizations for acute bleeding from esophageal varices have been declining in recent years, believed to be a result of more active primary and secondary prophylaxis. Bleeding occurs when the tension in the venous wall leads to rupture, and shock may occur. Occasionally, the bleeding may stop spontaneously, but more often the bleeding will recur. Thrombocytopenia and impaired hepatic synthesis of coagulation factors both interfere with hemostasis. Treatment includes pharmacologic, endoscopic, and radiologic shunting and surgery. Once large varices are identified, patients should begin -blocker therapy, such as propranolol, which reduces portal pressure and variceal blood flow and decreases risk of bleeding by 50%. Hepatic venous pressure measurements are used to monitor the success of this combination pharmacologic therapy, shown to be superior to sclerotherapy and possibly superior to band ligation. A recent meta-analysis showed that a combination of endoscopic and pharmacologic therapy reduces overall and variceal rebleeding in cirrhosis more than either therapy alone. If -blockers are not tolerated or are contraindicated, or if patients are at high risk for bleeding, endoscopic band ligation is preferred over sclerotherapy because of fewer complications and lower cost. Surveillance of varices, with potential rebanding, should be repeated every 6 months. Bleeding requires simultaneous control, resuscitation, and prevention/treatment of complications. Medical treatment of bleeding with vasopressin, terlipressin, somatostatin, or octreotide is started. These medications stop the bleeding in 65% to 75% of patients, but 50% will bleed again within a week. Vasopressin is a posterior pituitary hormone that constricts splanchnic arterioles and reduces portal flow and pressure. Definitive therapy is first performed with sclerotherapy or band ligation, which is successful in 90% of patients. Patients with acute variceal bleeding have hemodynamic instability (61%), tachycardia (22%), hypotension (29%), and orthostatic hypotension (10%). Screening should be performed for patients with low platelet counts, splenomegaly, or advanced cirrhosis. Endoscopy should also be performed for any patient who has hemorrhage of unexplained cause. In 25% of patients with varices that bleed, the cause is something other than varices. Esophageal varices are believed to be the cause of bleeding if no other source of bleeding is found. Other causes include gastric or duodenal ulcers, gastritis, Mallory-Weiss tear, and gastric varices. At endoscopy, the varices are blue, round, and surrounded by congested mucosa as they protrude into the lumen of the distal esophagus. They are soft and compressible, and an esophagoscope can be passed easily beyond them. Erosion of the superficial mucosa, with an adherent blood clot, signifies the site of a recent hemorrhage. However, recurrence is common before complete obliteration, and esophageal strictures typically develop. Endoscopic band ligation results in fewer strictures and ulcers than sclerotherapy and faster eradication. When bleeding is under control, endoscopic ligation and sclerotherapy are repeated every 1 to 2 weeks until the varices are eradicated. This technique has the fewest complications and the lowest incidence of recurrence. Surveillance is performed at 3- to 6-month intervals to detect and treat any recurrence. Patients who have two or more rebleeding episodes should be considered for surgery or transplantation. Balloon tamponade is used as a bridge to definitive therapy in 6% of patients when hemostasis is not achieved. Bleeding stops in 80% to 90% of patients, but unfortunately, 60% of them have recurrences. A new method involves the use of a self-expanding stent to stop acute bleeding from esophageal varices; initial studies reveal no method-related mortality or complications. Patients must be followed closely because the shunt may occlude in up to 50% of cases within 18 months. Shunt procedures are not the modality of choice because they result in a high rate of complications compared with medical therapy. Emergency bleeding may be controlled with a central portacaval shunt or with combined esophageal transaction, gastric devascularization, and splenectomy in patients hopeful for liver transplantation. Surgical shunts should be used to prevent rebleeding in patients who do not tolerate, or who are noncompliant with, medical therapy and who have relatively preserved liver function. Portal decompression procedures create a connection between the high-pressure portal and the low-pressure systemic venous systems. Selective shunts, such as the distal splenorenal shunt, only decompress esophageal varices. Elective shunt procedures are avoided in candidates for liver transplantation but may be performed in those with Child A and B cirrhosis. Liver transplantation is the best therapy for patients with Child C cirrhosis and is performed in only 1% of patients. Early complications after acute variceal bleeding include esophageal ulceration (2%-3% of patients), aspiration (2%-3%), medication adverse effects (0%-1%), dysphagia and odynophagia (0-2%), encephalopathy (13%-17%), and hepatorenal syndrome (2%). The prognosis for patients with bleeding esophageal varices depends directly on liver function. However, in patients with cirrhosis who have variceal bleeding, mortality risk is as high as 60% at 1 year. Zaman A: Current management of esophageal varices, Curr Treat Options Gastroenterol 6:499-507, 2003. Zehetner J, Shamiyeh A, Wayand W, et al: Results of a new method to stop acute bleeding from esophageal varices: implantation of a self-expanding stent, Surg Endosc 22(10):2149-2152, 2008. Patients may also have atypical symptoms and may consult several physicians before the correct diagnosis is established. The esophageal muscle works to clear the lumen of both acid and duodenal contents. Poor luminal clearance increases the exposure time, allowing previously healthy epithelium to become damaged tissue. The presence of bile, pepsin, and pancreatic enzymes in addition to acid indicate a more destructive atmosphere and therefore more severe disease. This ultrastructural abnormality is detected on transmission electron microscopy and light microscopy. Diagnostic testing should be done for patients with persistent symptoms who are already receiving therapy; those with recurrent symptoms, weight loss, dysphagia, or gastrointestinal bleeding; and those at risk for complications of esophagitis, as indicated by stricture formation, Barrett esophagus, and adenocarcinoma. Diagnosis depends on a combination of radiologic, pathologic, physiologic, and endoscopic findings. Tests are selected based on the information needed and may include esophageal pH monitoring, impedance testing, acid provocation tests, modified barium swallow, and endoscopy. Endoscopy is the preferred method to diagnose reflux or hiatal hernia, to grade esophagitis, and to obtain a biopsy sample of the esophagus to rule out Barrett esophagus or cancer. Among the classification systems used to grade disease severity, the Los Angeles Classification is the most widely accepted. The test measures realtime acid exposure and the ability of acid to clear the esophagus, correlating symptoms with acid exposure. Six determinants are used to calculate a DeMeester score: total time of reflux, upright time, supine time, number of episodes, number of episodes longer than 5 minutes, and longest episode. The Bravo pH monitoring system (Medtronic, North Shoreview, Minn) is an endoscopically placed device that measures 24-hour pH without the need for a nasogastric tube. Electrical impedance is the converse of conductivity and decreases from air to mucosal lining, to saliva, to swallowed material, and finally to refluxed gastric contents (lowest impedance). Using multiple impedance detection sites on a single catheter reveals the direction of bolus movement. It is a burning sensation in the chest or epigastrium caused by stomach acid, which rises into the esophagus. Of American adults, 44% experience heartburn monthly, 18% weekly, and 5% to 10% daily. Recent data support that being overweight, or even moderate weight gain among persons of normal weight, may cause or exacerbate symptoms of reflux. Atypical or extraesophageal symptoms include noncardiac chest pain, choking, laryngitis, coughing, wheezing, difficulty breathing, sore throat, hoarseness, asthma, and dental erosions. Physiologic changes caused by asthma and chronic cough cause airway inflammation and may promote acid reflux. This involves nerve reflexes, cytokines, inflammatory and neuroendocrine cells, and occasionally tracheal aspiration of refluxed gastric contents. The ciliated epithelium of otolaryngeal structures is more susceptible to damage from refluxate, which can occur from fewer and briefer episodes. The severity of symptoms is not a reliable indicator of the severity of erosive esophagitis. Recent studies reveal that 60% of reflux episodes are not conventional and can be detected only by impedance changes, not by 24-hour pH testing.

Such individuals may be brought into the hospital in a state of profound shock requiring immediate blood and fluid replacement before definitive surgical treatment can be instituted antifungal krem order cheap butenafine line. In adults fungus gnats gnatrol butenafine 15 mg order with amex, common sites of lacerations are the vaginal wall fungus under ring butenafine 15 mg purchase fast delivery, the lateral fornices fungus key buy butenafine with a visa, and the cul-de-sac fungus documentary discount butenafine online amex. Rape injuries are dangerous in elderly, postmenopausal women who, because of vulvar and vaginal atrophy and the attendant increased fragility of the vaginal wall, are predisposed to more extensive damage. In younger women, the trauma to the vagina from rape is usually not so grave, although during pregnancy and in the immediate postpartum period, the tissues are vascular, delicate, and liable to injury. Vigorous self-instrumentation during masturbation occasionally causes vaginal lacerations in children or older women, especially when a sharp or breakable object is used. Similarly, some practices in association with a sexual partner may result in accidental injury. Because of its relatively protected position between the thighs and inside the external genitalia, the vagina is seldom subject to trauma by other than sexual means. When it does occur, it is most frequently the so-called picket fence injury caused by falling astride a sharp object that penetrates the vagina. In the lower picture, the arrows indicate the various possible lines of perforation, and it must be remembered that the lesions may be multiple. The spike of the metal fence has passed upward through the vagina, lacerating the posterior wall and piercing the peritoneum of the posterior cul-de-sac. There are three basic responsibilities in the care of someone who may have been raped or abused: the detection and treatment of serious injuries, the preservation of evidence, and protection against sequelae. The latter may involve several different stages, depending on which organs are involved, but the steps can be taken in logical sequence once the patient has been made safe for surgery. There is some experimental evidence that changes in gene activation after childbirth can affect elastin production and repair, increasing the risk of pelvic support defects. Small cystoceles, involving only a slight deviation from the normal, are referred to as first degree; those that advance nearly to the introitus are second degree; those that come to the introitus or beyond are third degree. Other classifications use a four-step designation with the differentiation between the third and fourth degrees being the level of the hymenal ring. Cystocele and urethrocele can be demonstrated by pressing against the perineum of a patient in the lithotomy position and having her strain. An evaluation of urinary function is advisable, especially if surgical therapy is being considered. Anterior support failures are best demonstrated by having the patient strain or cough while observing the vaginal opening through the separated labia. A Sims speculum or the lower half of a Graves, Peterson, or other vaginal speculum may be used to retract the posterior vaginal wall, facilitating the identification of the support defect. Specific measures include pessary therapy, pelvic muscle exercises, and surgical repair. The clinical end result of posterior obstetric trauma may be a rectocele or enterocele. They can ensue after multiple pregnancies in the absence of severe trauma or, as in cystocele, from any situation that tends to increase the intraabdominal pressure over a long period of time. Congenital weakness, poor health, and poor care predispose to the development of rectocele. A rectocele may be found in 10% to 15% or women, rising to 30% to 40% of women after menopause. Hemorrhoids, prolapse of the rectal mucosa, and local infections about the anus may occur in association with large rectoceles. Surgical repair is indicated when the hernia causes severe symptoms or is of very large size. It is usually done for first- or second-degree rectocele in the course of a vaginal plastic operation devised primarily for cystocele and uterine prolapse, because good levator approximation further buttresses the anterior wall. Congenital elongation of the cul-de-sac of Douglas with prolapse of the intestine or omentum can produce inversion of the pelvic floor in the absence of obstetric trauma in the condition known as primary enterocele. Palpation of intraperitoneal structures and the presence of peristaltic activity in the sac are more conclusive evidence. Such recurrences are referred to as secondary enteroceles, but in those cases that have had previous inadequate surgical treatment of a primary enterocele, the term is a misnomer. These fistulae may occur in any part of the vaginal canal and are sometimes multiple. Urinary tract fistulae may result from surgical or obstetric trauma, irradiation, or malignancy, although the most common cause by far is unrecognized surgical trauma. Urinary tract fistulae are most common after uncomplicated hysterectomy, although pelvic adhesive disease, endometriosis, or pelvic tumors increase the individual risk. More severe defects should not be repaired until the tissues have returned to normal condition. Cystoscopy may be required to evaluate the location of a urinary tract fistula in relation to the ureteral opening and bladder trigone and to exclude the possibility of multiple fistulae. Vesicocervicovaginal fistulae are relatively uncommon and are usually caused by cancer of the cervix or surgical injury to the bladder in the course of a subtotal hysterectomy. Inflammatory bowel disease or pelvic radiation therapy may hasten or precipitate fistula formation. Surgical treatment of these defects is complicated, because the underlying pathologic process is usually still progressing and the results are poor. Ureterovaginal fistulae are of serious significance because measures to restore the continuity of the urinary tract may be unsuccessful with loss of the involved kidney. This decrease has just as an important effect upon the vulvar and vaginal tissues as upon the uterine lining. This is a normal physiologic process and, in the early stages, may give rise to no subjective manifestations, although it can usually be observed clinically as a general shrinking in the caliber of the vaginal canal, with shortening of the fornices. The rugae become less prominent, and the epithelium is of a pale rather than a rosy hue and is increasingly friable. There is a change in vaginal pH toward the alkaline as the normal vaginal flora are lost. The histology of the vagina after the menopause is characterized by a thin superficial epithelium. In the subepithelium is found a diffuse infiltration of both polymorphonuclear leukocytes and lymphocytes. Clinically, the condition may be confused with a Trichomonas infection, and infestation with T. Almost any type of bacterial organism may be involved, and the infection is usually mixed. The latter is to be particularly avoided during pelvic examinations on elderly women or in the course of a vaginal preparation for an operative procedure. Care must be exercised with topical therapy in these patients, for up to 25% of estrogen placed in the vagina may be absorbed into the circulation. Vaginal cysts are formed chiefly from embryonic epithelial remnants, which may be derived from either the müllerian or wolffian ducts, the latter giving rise to the Gartner duct cysts found on the anterolateral vaginal walls. Occasionally, a cyst of this type is large enough to occlude the vaginal canal and resemble a cystocele. Because the wolffian duct crosses the anlagen of the broad ligament and the uterus before entering the anterolateral vaginal wall, it is not unusual for cysts of mesonephric origin to extend well upward between the leaves of the broad ligament, increasing the hazard of surgical excision. These cysts, often an incidental finding on routine pelvic examination, need not always be excised, although some uncertainty as to the exact histologic nature of the lesion must exist when the physician decides on conservative management. Some inclusion cysts are formed when the adult vaginal epithelium is turned into the subepithelial tissues as a result of the trauma of delivery or vaginal surgery. Inclusion cysts average less than 1 cm in diameter and are seldom larger than 3 cm. Multiple Gartner duct cysts Inclusion cyst Condylomata acuminata Fibroma Papilloma and condylomata acuminata occur in the vagina as well as on the external genitalia. They produce a foul discharge, especially when they become large and infected, and must be carefully differentiated from malignancy and the venereal granulomas before appropriate treatment is instituted. Local application of podophyllin, trichloroacetic acid, or other topical therapies eradicates the majority of small lesions. Fibroma and myoma are quite common in the vagina but are seldom of a size sufficient to produce symptoms. It is most common during the third and fourth decades of life, with 5% of cases diagnosed after menopause. Typical blue-domed endometrial cysts extend down the rectovaginal septum, causing agglutination of the anterior rectal wall to the posterior surface of the uterus. The presence of endometrium in the septum and its response to the cyclic influence of the ovarian hormones produce a dense, fibrous reaction, which is technically difficult to manage during surgery. The aberrant endometrium rarely penetrates the anterior rectal wall to involve the mucous membrane but more often invades the posterior vaginal fornix. Although the occurrence of endometriosis is understandable in areas where coelomic metaplasia or gravitational fall of regurgitated endometrial particles may be the exciting cause, its growth in areas far removed from the pelvis is harder to explain. In the former case, it is assumed that migration is downward through the canal of Nuck, because this tube is lined by coelomic epithelium; but in the perineum, such an explanation does not hold. Perhaps, in this instance, the spread of endometrium has been by way of the pelvic lymphatics, as suggested by Halban. In the absence of external endometriosis elsewhere, local excision of this lesion is indicated, if only for purposes of accurate microscopic diagnosis. The lesion is most often located on the posterior vaginal wall and in the upper half of the vagina. The differential diagnosis must exclude the venereal granuloma and the possibility that the tumor is secondary. Radiation is probably the best overall type of therapy except in very early stage disease. Radium needles can be inserted interstitially and should be followed by deep x-ray therapy to the pelvis. The 5-year salvage following either form of treatment is very low when the tumor is advanced. Growth proceeds by direct extension to involve the entire vagina, but hematogenous spread may also occur, with metastases to the lungs and other distant organs. Microscopically, these sarcomas may be of spindle cell, round cell, or mixed cell types. A rare form of sarcoma (embryonal rhabdomyosarcoma) is generally found in the vagina of young girls. The relatively high incidence of secondary lesions is due chiefly to the frequent extension of carcinomas of the cervix to the adjacent vaginal epithelium and supporting structures. By convention, tumors involving the vagina and cervix are classified as cervical in origin; tumors involving the vulva and vagina are similarly classified as vulvar in origin. The vagina is the most frequent site of metastases from uterine chorionepithelioma, and a speculum view of the dark-purple hemorrhagic growth is often the earliest manifestation of the presence of this disease. A biopsy of this lesion shows the unmistakable alveolar arrangement of the large, pale-staining cells. A virtually unique vaginal metastatic malignancy is the case of a carcinoma of the thyroid that metastasized to the rectovaginal septum. Pigmented vaginal lesions may occur, including nevi and melanoma, which account for 9% of vulvar and 5% of vaginal malignant lesions. Prognosis and therapy of these lesions is predicated on the site and stage of the originating lesion. Metastases or extensions from carcinomas of the ovary, bladder, or rectum are found in the vagina either before or after treatment of the primary disease. It would be unlikely that these extensions would provide the first indication of disease, but nearly all secondary vaginal neoplasms cause foul leukorrhea and bleeding and, if unchecked, may eventually produce urinary or fecal fistulae. The viscera contained within the female pelvis minor include the pelvic colon, urinary bladder and urethra, uterus, uterine tubes, ovaries, and vagina. As with the pictures illustrating the structures of the male pelvis, the topography of the female pelvis is demonstrated in two sections. Its greater part lies in a horizontal plane, though it may occupy many positions, including the superior surface and posterior aspect of the uterus. The rectum extends from the third sacral vertebra to just beyond the tip of the coccyx. It is covered by peritoneum in front and at the sides in its upper third and in front only in its middle third; its lower third is devoid of peritoneum. The ureter then ascends in front of the vagina for a short distance to reach the base of the bladder, where it opens into the lateral angle of the trigone by piercing the bladder wall obliquely. The urinary bladder lies behind the symphysis, in front of the uterus and the vagina. The neck of the bladder lies on the superior surface of the urogenital diaphragm and is continuous with the urethra. The superior surface is covered by peritoneum and is in contact with the body and fundus of the anteflexed uterus. It is this reflection that must be mobilized during the course of cesarean delivery. The anterior surface is flat and looks downward and forward, resting on the bladder. The peritoneum of the posterior wall covers the body and upper cervix and then extends over the posterior fornix of the vagina to the rectum, to form the rectouterine pouch or cul-de-sac of Douglas. The external os of the cervix lies at about the level of the upper border of the symphysis pubis in the plane of the ischial spine. At the points where these hollow organs pierce the pelvic floor, tubular fibrous investments are carried upward from the superior fascia as tightly fitting collars, which blend with and may even become inseparable from their outer muscle coat. Thus, three tubes of fascia are present, encasing, respectively, the urethra and bladder, the vagina, and the lower uterus and the rectum.

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