Disorders of the Chest Wall, Diaphragm and Spines

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Information about Disorders of the Chest Wall, Diaphragm and Spines

Published on May 18, 2012

Author: drriham

Source: authorstream.com

Disorders of the Chest Wall, Diaphragm, and Spine: Disorders of the Chest Wall, Diaphragm, and Spine By Chest Department Ain Shams University Nonmuscular Diseases of the ChestWall: Nonmuscular Diseases of the ChestWall The chest wall, an integral part of the respiratory pump, consists of the rib cage, rib cage muscles, diaphragm, and abdomen. Like the respiratory muscles, the nonmuscular structures of the chest wall (i.e., thoracic spine, ribs) are also essential for normal respiratory function. Disorders primarily affecting these structures, by themselves or in combination with other disease processes, may impose elastic and resistive loads on the inspiratory muscles, weaken them and ultimately lead to respiratory failure and death. KYPHOSCOLIOSIS: KYPHOSCOLIOSIS Diagnosis and Etiology Kyphoscoliosis refers to a group of spinal disorders characterized by curvature of the spine in the lateral direction (scoliosis),sagittal plane (kyphosis) as well as rotation of the spine itself. Kyphoscoliosis may be: (a) congenital; (b) secondary to other disorders; or (c) idiopathic. Congenital kyphoscoliosis is usually present at birth. Not necessarily familial, congenital kyphoscoliosis may be related to isolated malformations of the vertebrae during prenatal development or may be a manifestation of a more generalized disorder such as muscular dystrophy, or neurofibromatosis. Secondary kyphoscoliosis is usually associated with diseases that primarily affect the neuromuscular system. Kyphoscoliosis associated with neuromuscular disease is sometimes referred to as “paralytic” kyphoscoliosis. The most common causes of paralytic kyphoscoliosis are polio, muscular dystrophy, cerebral palsy, and spina bifida. Idiopathic kyphoscoliosis, the most common late childhood or early adolescence and involves females more often than males with a ratio of 4:1. Causes of Kyphoscoliosis: Causes of Kyphoscoliosis Congenital Paralytic or secondary Neuromuscular Poliomyelitis Muscular dystrophy Cerebral palsy Friedreich’s ataxia Charcot-Marie-Tooth disease Disorders of connective tissue Marfan’s syndrome Ehlers-Danlos syndrome Morquio’s syndrome Vertebral disease Osteoporosis Osteomalacia Vitamin D-resistant rickets Tuberculous spondylitis Spina bifida Post-thoracoplasty Idiopathic PowerPoint Presentation: In severe kyphoscoliosis, the deformity is readily apparent on physical examination. However, the true degree of spinal rotation and flexion is not apparent on physical examination, especially in mild cases. The severity of the defect is more accurately assessed by radiographically measuring the Cobb angle, which is the angle formed by the intersection of two lines, each of which is parallel to the top and bottom vertebrae of the scoliotic or kyphotic curves. The greater the Cobb angle, the more severe is the deformity. Cobb angles of greater than 100 degrees are more likely to be associated with respiratory symptomatology. Typically, symptoms consist of dyspnea on exertion that progress with age and the degree of spinal deformity. Respiratory Mechanics and Pulmonary Function Tests : Respiratory Mechanics and Pulmonary Function Tests The combined effects of kyphosis, scoliosis, and rotation of the spine reduce the compliance of the chest wall and increase the recoil pressures of the chest wall and the respiratory system at any given lung volume, with the recoil pressures being greatest as one approaches total lung capacity (TLC). Respiratory muscle strength, assessed by (PImax and PEmax), may be normal or reduced in patients with kyphoscoliosis. Kyphoscoliosis can lead to one of the most profound restrictive patterns of any of the chest wall diseases. TLC and vital capacity (VC) may be reduced to 30 % of predicted with severe deformities of the spine. Residual volume (RV) may be normal or slightly increased. Since the RV is not as severely affected as TLC, the RV/TLC ratio may be high. Individuals with mild and moderate degrees of kyphosis and scoliosis (Cobb angles less than 60 degrees) may only have mild reductions in VC and TLC. Individuals with Cobb angles greater than 90 degrees, however, invariably have restricted lung volumes. PowerPoint Presentation: Other factors contributing to the degree of restriction include: (a) the number of vertebrae involved; (b) the location of the curve; (c) the patient’s age;(d) the presence of kyphosis; and (e) the degree of rotation of the spine. Although indices of forced expiratory flow are typically reduced, i.e. a low FEV1, the ratio of FEV1/FVC remains normal, thereby indicating no concomitant obstructive process. The combination of reduced chest wall and lung compliance increases the elastic work of breathing. Since the oxygen cost of breathing increases with increasing loads placed on the respiratory system, it is not surprising that the resting oxygen cost of breathing is three to five times that seen in healthy subjects. Inspiratory muscle weakness diminishes respiratory muscle reserve by reducing maximal forces and velocities of shortening that the muscles can develop. Since respiratorymuscle fatigue is, in part, a function of the balance between the loads placed upon the respiratory muscles and their reserve to overcome these loads, it is clear that individuals with severe kyphoscoliosis are at high risk for developing respiratory failure. Exercise Capacity:: Exercise Capacity: Individuals with combined restrictive defect and inspiratory muscle weakness have impaired exercise tolerance. Maximum oxygen consumption may be reduced to about 60 to 80 % of predicted. Because these individuals exhibit a restrictive pattern on pulmonary function testing, the breathing pattern response to exercise in patients with severe kyphoscoliosis differs from that seen in normal subjects. Specifically, the ratio of tidal volume to vital capacity (VT/VC) is greater than 0.5 and the ratio of maximum exercise ventilation to maximum voluntary ventilation (VEmax/MVV) can reach 70 % . Deconditioning and lack of regular aerobic exercise may be contributing to the poor exercise tolerance in individuals with moderate to severe scoliosis. Supplemental oxygen may improve oxygenation during exercise but usually does not affect walk distance. Sleep Disordered Breathing: Sleep Disordered Breathing Patients with kyphoscoliosis may be predisposed to hypoventilation during sleep. the degree of oxyhemoglobin desaturation during sleep is more severe in individuals with severe kyphoscoliosis than that seen during sleep in patients with other respiratory diseases. Because sleep-related disorders represent a potentially treatable cause of respiratory failure, they should always be evaluated in kyphoscoliotic patients with carbon dioxide retention. Gas Exchange: Gas Exchange Persistent nocturnal desaturation may eventually be associated with daytime hypoxemia and hypercapnia. The cause of hypoxemia may be multifactorial; ventilation/perfusion (V/Q) mismatching is commonly present and is worse in patients with Cobb angles greater than 65 degrees. Intrapulmonary shunt related to underlying atelectasis as well as alveolar hypoventilation may also account for the hypoxemia in some individuals. Hypercapnia initially appears during sleep and with exercise; eventually,as the disease progresses, hypercapnia is seen during the day. Prolonged hypoxemia may result in pulmonary hypertension. The degree of hypoxemia is positively associated with the degree of kyphosis, but not with the etiology of kyphoscoliosis,or age of onset of scoliosis. Individuals with severe kyphoscoliosis may have oxyhemoglobin desaturation with minimal activity. Clinical Course: Clinical Course Congenital kyphoscoliosis may exhibit a rapidly progressive course with spinal cord compression further compromising the respiratory system. Similarly, individuals with neuromuscular disease who develop secondary kyphoscoliosis may also have pronounced respiratory disability. Those at greater risk for developing respiratory complications are individuals who have an onset of the spinal deformity at an early age, rapid progression of the deformity during growth, and continued progression after skeletal maturity. By contrast, individuals with idiopathic kyphoscoliosis typically have a more benign course. If the thoracic deformity is mild, they have an excellent prognosis with little impairment in breathing or overall lifestyle. Individuals with mild idiopathic kyphoscoliosis are no more likely to develop ventilatory failure or have any greater loss of lung volume with aging than the general population. However, those with moderate or severe idiopathic kyphoscoliosis may be at higher risk for respiratory compromise.In general, individualswith thoracic deformities greater than 50 degrees at skeletal maturity are at risk for a progressive increase in the spinal angulation at a rate of about 1 degree annually. Treatment: Treatment General supportive care for adults with kyphoscoliosis includes immunization against influenza and pneumococci,prompt care of respiratory infections, use of supplemental oxygen, smoking cessation, and maintenance of body weight within a desirable level. Preventive measures include interventions such as chest physiotherapy, use of bronchodilators,diuretics, and physical activity to improve exercise capacity and minimize deconditioning. Supplemental oxygen may be needed with activity or exercise and can be beneficial in improving exercise tolerance. Specific treatment of nocturnal hypoventilation can be accomplished with noninvasive positive pressure ventilation, which is typically delivered by a nasal or full-face mask. Indications for initiating noninvasive nocturnal ventilation include symptoms suggestive of nocturnal hypoventilation (i.e., fatigue, morning headache, dyspnea) or signs of cor pulmonale with either an elevated daytime arterial Pco2 or nocturnal oxygen saturation less than 88 percent for 5 consecutive minutes. PowerPoint Presentation: Operative treatment traditionally consists of spinal fusion and/or insertion of Harrington rods. These approaches have been used for many years to correct the spinal deformity and stabilize the spine. However, these interventions are often accompanied by complications later in life, such as chronic back pain or further spinal deformation. Surgery has recently evolved to include less invasive procedures such as titanium rib implantation with rib cage expansion. Initial results are promising in individuals with congenital kyphoscoliosis. THORACOPLASTY: THORACOPLASTY Thoracoplasty consists of different combinations of rib removal, rib fractures, phrenic nerve resection, or compression of underlying lung by filling the pleural space with foreign material. These individuals commonly developed dyspnea, severe restrictive dysfunction, and chronic respiratory failure as they aged. The severity of the restrictive pattern was related to a number of factors including: the number of ribs removed, the presence of fibrothorax, progressive lung fibrosis due to underlying granulomatous disease, previous lung resection, or phrenic nerve damage. Often, surgery on the rib cage was followed by progressive scoliosis with aging and further deterioration of respiratory function. The severity of restriction and stiffening of the chest wall was similar to that seen with kyphoscoliosis leading to an increase in the oxygen cost of breathing, limited exercise tolerance, and impairment in gas exchange. PowerPoint Presentation: Chest radiograph of a patient with a history of M. tuberculosis demonstrating marked deformity of the left hemithorax consistent with prior thoracoplasty. PECTUS EXCAVATUM: PECTUS EXCAVATUM Pectus excavatum is a chest wall deformity characterized by excessive depression of the sternum which affects between 0.5 and 2 %of the population. The deformity occurs more frequently in males than females (3:1 ratio). The sternal depression can be minimal or extreme. The etiology of pectus excavatum is unknown. It is possible that a defect in the connective tissues surrounding the sternum may be present. Connective tissue disorders such as Marfan ’ s syndrome have a higher incidence of pectus deformity. A family history may or may not be present and other factors such as scoliosis, congenital heart disease, and functional heart murmurs occur in patients with pectus excavatum. The most frequent complaints are cosmetic. Dyspnea with activity and exercise intolerance occurs in 30 to 70 % of patients. Although rare, respiratory failure can occur in adults with severe pectus deformity. The degree of deformity is assessed radiographically, mainly by (CT). Respiratory Mechanics and Exercise Capacity : Respiratory Mechanics and Exercise Capacity Impairment in pulmonary function is usually minimal, with TLC and VC being normal or mildly reduced. In most cases, there is no underlying lung disease and lung compliance is normal. If restriction is apparent on pulmonary function testing, it may be related to the presence of concomitant scoliosis. In contrast to individuals with ankylosing spondylitis, the mobility of the rib cage is not impaired during quiet breathing or exercise. Treatment Medical therapy for pectus excavatum is generally supportive. The surgical approaches may be invasive or minimally invasive. Physiological benefits of either invasive or minimally invasive procedures remain controversial. ANKYLOSING SPONDYLITIS: ANKYLOSING SPONDYLITIS Ankylosing spondylitis (AS), a chronic inflammatory disease of unknown etiology, is the prototype of a group of related disorders known as the spondyloarthritides, the main characteristic of which is inflammation of the axial skeleton. The spinal involvement in AS can be more severe than that seen in other spondyloarthritides. Clinically , AS patients typically complain of low back pain and stiffness beginning in late adolescence or early adulthood; onset of the disease after the age of 45 is rare. Symptoms are worse in the morning or after rest. Chest pain due to inflammation of manubriosternal junction and/or the sternoclavicular joints and inability to fully expand the chest on inspiration are infrequent complaints. On physical examination , there may be tenderness of the anterior chest wall, or over the costochondral region or the manubriosternal junction. Exercise intolerance and dyspnea are uncommon Respiratory Mechanics and Pulmonary Function Tests : Respiratory Mechanics and Pulmonary Function Tests Limited expansion of the rib cage is the hallmark of respiratory involvement in AS. Mild reductions in VC and TLC both FRC and RV may be increased above predicted normal levels; consequently, the RV/TLC ratio may also be higher. Osteoporosis of the thoracic spine, which is frequently found in AS, especially in late stages, may lead to kyphosis, modest spinal deformity, and worsening of the restrictive defect .Cervical spine fractures, usually at the C6 or C7 level, can result in tetraplegia and respiratory failure. They are associated with a high mortality. Gas exchange is usually normal, with Pao2 either within the normal range or slightly reduced. Exercise capacity may be mildly decreased. Treatment Medical treatment to relief symptoms and. Physiotherapy is regarded as an essential element of the overall management in AS. The recent introduction of antagonists of tumor necrosis factor (TNF) shown remarkable improvements in all aspects of the disease, including rib cage expansion and quality of life. An adverse effect of the anti-TNF therapy may be reactivation of tuberculosis. FLAIL CHEST: FLAIL CHEST Flail chest can occur in up to 25 % of adults who have blunt chest wall trauma. It is a condition in which fractures of the ribs produce a segment of the rib cage that deforms markedly during breathing. Pulmonary complications such as pulmonary contusion, hemothorax, and pneumothorax can occur in up to 60 % of patients with flail chest. Thus, the mortality from flail chest may be high. Symptoms consist of chest tightness, chest pain, dyspnea, and limitation of ability to exercise. The disordered movement of the flail segment is related to changes in pleural pressure during the breathing cycle unopposed subatmospheric intrapleural pressure causes the flail segment to move inward during inspiration. During expiration, pleural pressure becomes more positive and the flail segment moves outward. This paradoxical motion of the flail segment is amplified by anything that further lowers pleural pressure, such as pulmonary contusion, which reduces lung compliance or an increase in airway secretions, which increases airways resistance. Flail chest may severely reduce VC and FRC to as much as 50 % of predicted. Treatment : Treatment The mainstay is pain control to reduce splinting, improve tidal volume, and minimizes areas of atelectasis. It can be accomplished by use of oral or intravenous narcotics, intercostal nerve blocks, or epidural anesthesia. Supplemental oxygen, improving tracheal bronchial toilet are used. Mechanical ventilation with positive pressure breathing has been shown to stabilize the flail segment by eliminating subatmospheric changes of pleural pressure during inspiration. However, complications of mechanical ventilation often supervened and increased morbidity and mortality. Consequently, mechanical ventilation is no longer recommended as a primary means of stabilizing the chest wall; instead, it is recommended when there is respiratory failure ,or other indications. Positive pressure ventilation delivered by noninvasive techniques may provide an alternative means by preventing subatmospheric changes in pleural pressure during inspiration. Noninvasive ventilation to selected patients who are breathing spontaneously in conjunction with regional anesthesia can improve gas exchange and enable physiotherapy and early patient mobilization. PowerPoint Presentation: Levels of Respiratory System Dysfunction Induced by Neuromuscular Diseases and Conditions Level Disease or Condition Upper motoneuron Cerebral Vascular accidents Cerebellar atrophy Trauma Spinal cord Trauma Tumor Syringomyelia Multiple sclerosis Lower motoneuron Anterior horn cells Poliomyelitis Spinal muscle atrophy Amyotrophic lateral sclerosis Motor nerves Cardiac surgery Charcot-Marie-Tooth disease Diabetes Polyneuropathy Toxins PowerPoint Presentation: Guillain-Barr ´e syndrome Neuralgia amyotrophy Critical illness polyneuropathy Neuromuscular Myasthenia gravis junction Eaton-Lambert syndrome Botulism Organophosphate poisoning Drugs Muscle Dystrophy Acid maltase deficiency Malnutrition Corticosteroids Polymyositis Diaphragm Paralysis: Diaphragm Paralysis Unilateral or bilateral diaphragm paralysis following phrenic nerve injury can result from cardiac surgery, trauma, mediastinal tumors, infections of the pleural space, or forceful manipulation of the neck. Phrenic nerve injury during open heart surgery is one of the most common causes of unilateral and bilateral diaphragm paralysis and is due either to cold exposure during cardioplegia or to mechanical stretching of the phrenic nerve during surgery. Diaphragm paralysis may also be seen with a variety of motoneuron diseases ,myelopathies, neuropathies, and myopathies. Bilateral diaphragm paralysis is characterized by a severe restrictive ventilatory impairment, with VC being frequently less than 50 % of predicted in the upright position and a further reduction of 25 % or more in VC in the supine position. TLC is also markedly decreased, as well as FRC and static pulmonary compliance. In most patients with non traumatic bilateral diaphragm paralysis, the most important clinical feature is orthopnea out of proportion to the severity of the underlying cardiopulmonary disease. PowerPoint Presentation: In patients with non traumatic bilateral diaphragm paralysis, the diaphragm usually goes unrecognized until they present with cor pulmonale or cardiorespiratory failure. A chest radiograph showing elevation of both hemidiaphragms with volume loss and/or atelectasis at the lung bases is common. With diaphragm paralysis, a marked reduction in PImax with preservation of PE max should be found, and in general, there is a correlation between maximum inspiratory pressures and Pdi sniff. Reductions in Pdi sniff to less than 30 cmH2O are accompanied by orthopnea, a supine decrease in VC, and the presence of abdominal paradox. In most cases, the presence of severe bilateral diaphragm weakness can be diagnosed from physical exam, measurements of VC in the upright and supine positions, and PImax and PEmax. An elevation in PaCO2, particularly in the supine position in patients with diaphragm paralysis has been reported PowerPoint Presentation: Treatment of patients with bilateral diaphragm paralysis is similar to that of other patients with chronic neuromuscular diseases. Eliminating nocturnal hypoventilation, especially during REM sleep is warranted, and the implementation of noninvasive ventilation, especially positive-pressure ventilation, may be indicated. In some cases of symptomatic unilateral hemi diaphragm elevation, surgical plication of the affected hemi diaphragmmay relieve symptoms and improve FVC and trans- diaphragmatic pressure. Guillain-Barr ´e Syndrome: Guillain-Barr ´e Syndrome GBS precipitates respiratory failure more often than any other peripheral neuropathy. It is an acute idiopathic polyneuritis. It usually presents as paresthesia and ascending paralysis of the lower extremities with absent deep tendon reflexes in a symmetrical distribution. Objective findings of sensory loss are variable, and the degree of motor weakness can range from mild paresis to complete paralysis. Maximum weakness of the lower extremities occurs within 2 weeks in 50 % of cases, and 90 % of cases reach their maximum weakness by 4 weeks. After the nadir is reached, patients remain at that level for an additional 1 to 4 weeks before recovery begins. Facial, ocular, and oropharyngeal muscles may be impaired as well as the respiratory muscles. Respiratory muscle weakness and, specifically, severe diaphragm weakness may be found in patients with GBS. The distribution of muscle weakness between respiratory and non respiratory muscles is not uniform in GBS, and peripheral muscle strength does not correlate with the presence or absence of respiratory muscle weakness. However, ventilatory failure correlates with diaphragmatic weakness. PowerPoint Presentation: The impairment on respiratory tests in GBS is similar to that for other generalized neuromuscular diseases. A decline in FVC and maximum inspiratory and expiratory mouth pressures, impairment in nocturnal gas exchange during REM sleep, and the onset of hypercapnia detected by arterial blood gas analysis have all been reported in symptomatic GSB patients. Earlier intubation and assisted ventilation may be indicated to avoid complications that arise from progressive respiratory failure, overwhelming pulmonary infections, or both. When indicated, intubation and mechanical ventilation should be initiated early because emergent intubations have been associated with worse outcomes. Plasmapheresis should be started within 2 weeks of the onset of symptoms or earlier, if possible. Intravenous immunogammoglobulin, given within 2weeks after the onset of GBS, may also be effective therapy. Myasthenia Gravis: Myasthenia Gravis Is an autoimmune disorder characterized by impaired transmission of neural impulses across the neuromuscular junction due to the production of antibodies directed against the acetylcholine receptor. The prevalence of myasthenia gravis is estimated to be approximately 1 in 10,000 people with 2-to-1 female-to-male predominance. It occurs more often in younger than older adults. The typical myasthenic patient presents with fluctuating muscular weakness, with improvement after rest and the administration of anticholinesterase agents. Ocular, facial, and neck muscles are commonly affected, but patients who have the most severe respiratory involvement have either acute fulminating or late severe classifications of myasthenia gravis. The most common complications of myasthenic crisis are respiratory failure and recurrent pneumonias due to aspiration from bulbar involvement and impaired cough. PowerPoint Presentation: Noninvasive bilevel (BiPAP) positive pressure ventilation is a viable option to treat respiratory failure during a myasthenic crisis until effective therapy is delivered. The treatment of myasthenia gravis includes anticholinesterase agents, high-dose corticosteroids, thymectomy, and plasmapheresis in patients refractory to steroid or immunosuppressive therapy. Principles of Management: Principles of Management Principles in management of respiratory dysfunction in patients with neuromuscular disease include: (a) preventive therapies designed to minimize the impact of impaired secretion clearance and alveolar hypoventilation on gas exchange and lower respirator tract infections; and (b) stabilization of patients who develop acute or chronic respiratory failure. Preventive Therapies : Intermittent Positive Pressure Breathing Respiratory Muscle Training Mechanical Ventilation Indications for Mechanical Ventilation in Patients with Neuromuscular Diseases:: Indications for Mechanical Ventilation in Patients with Neuromuscular Diseases: Acute respiratory failure Severe dyspnea Marked accessory muscle use Copious secretions Unstable hemodynamic state Hypoxemia refractory to supplemental O2 Acute severe gas exchange disturbances (increased PaCO2 with pH ≤7.25) Chronic respiratory failure Symptoms of nocturnal hypoventilation (e.g., morning headaches, decreased energy, nightmares, enuresis) Dyspnea at rest or increased work of breathing impairing sleep Cor pulmonale due to hypoventilation, PaCO2 > 45, pH < 7.32 after treating reversible conditions Nocturnal desaturation (SaO2 < 88%) despite supplemental O2 therapy Invasive Versus Noninvasive Mechanical Ventilation in Patients with Neuromuscular Disease: Invasive Versus Noninvasive Mechanical Ventilation in Patients with Neuromuscular Disease Noninvasive Ventilation (No Airway Cannulation ) Invasive Ventilation (Endotracheal orTracheostomy Tube & P-Pressure Ventilation ) Awake, cooperative patient Copious secretions Good airway control Inability to control upper airway Minimal secretions Inability to tolerate or failure of noninvasive ventilation Hemodynamic stability Impaired cognition Reversible cause of respiratory failure Unstable hemodynamics PowerPoint Presentation: Thank You

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