Diaphragm Disorders - (Print..

Diaphragm Disorders: [Print] - eMedicine Pulmonology
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Diaphragm Disorders
Abhijit A Raval, MD, Pulmonary Diseases and Critical Care Fellow, James H Quillen College of Medicine Ryland P Byrd Jr, MD, Professor, Department of Internal Medicine, Division of Pulmonary Medicine and Critical Care Medicine, James H Quillen College of Medicine, East Tennessee State University; Chief of Pulmonary Medicine, Medical Director of Respiratory Therapy, Intensive Care Unit, Program Director of Pulmonary Diseases and Critical Care Medicine Fellowship, James H Quillen Veterans Affairs Medical Center Updated: Feb 12, 2009
Introduction
Background
The diaphragm is the major muscle of respiration and separates the thoracic and abdominal cavities. The body relies on the diaphragm for normal respiratory function. Contraction of the diaphragm has following functions: (1) decreasing intrapleural pressure, (2) expanding the rib cage through its zone of apposition by generating positive intra-abdominal pressure, and (3) expanding the rib cage using the abdomen as a fulcrum.1 Therefore, understanding how different disease processes and disorders result in diaphragm dysfunction is important. A concomitant respiratory dysfunction exists any time a decrease in diaphragmatic function is present. The body possesses inherent mechanisms of compensation for decreased diaphragmatic function, but none of these processes can successfully prevent respiratory compromise if excursion of the diaphragm is moderately diminished or simply absent. The easiest approach to diaphragmatic problems is to observe both the neurologic and anatomic processes that result in decreased function. Neurologic problems of the diaphragm occur when a traumatic injury or disease process decreases or terminates the impulse of respiratory stimuli originating in the brain. Anatomic disorders decrease the integrity of the musculature of the diaphragm, thus decreasing its excursion. Both anatomic and neurologic problems related to the diaphragm ultimately result in the inability of the diaphragm to provide adequate negative intrathoracic pressure, thereby decreasing the amount of oxygen provided to the alveoli. Anatomy of the diaphragm The diaphragm is a modified half-dome of musculofibrous tissue that separates the thorax from the abdomen. The 4 embryologic components that make up the formation of the diaphragm are the septum transversum, 2 pleuroperitoneal folds, cervical myotomes, and the dorsal mesentery. Development begins during the third week of gestation and is complete by the eighth week. Failure in the development of the pleuroperitoneal folds and subsequent muscle migration results in congenital defects (see Disorders of anatomy in Pathophysiology). The muscular origin of the diaphragm is from the lower 6 ribs bilaterally, the posterior xiphoid process, and from the external and internal arcuate ligaments. A number of different structures traverse the diaphragm, but 3 distinct apertures allow the passage of the aorta, esophagus, and vena cava. The aortic aperture is the lowest and most posterior of the openings, lying at the level of the 12th thoracic vertebra. The aortic opening also transmits the thoracic duct and, sometimes, the azygous and hemiazygous veins. The esophageal aperture is surrounded by diaphragmatic muscle and lies at the level of the 10th thoracic vertebra. The vena caval aperture is the highest of the 3 openings and lies level to the disk space between the eighth and ninth thoracic vertebrae.
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Arterial supply to the diaphragm comes from the right and left phrenic arteries, the intercostal arteries, and the musculophrenic branches of the internal thoracic arteries. Some arterial blood is provided from small branches of the pericardiophrenic arteries that run with the phrenic nerve, mainly where the nerves penetrate the diaphragm. Venous drainage occurs via the inferior vena cava and azygous vein on the right and the adrenal/renal and hemizygous veins on the left. The diaphragm receives its sole neurologic impulse from the phrenic nerve, which originates primarily from the fourth cervical ramus but also has contributions from the third and fifth rami. Originating around the level of the scalenus anterior muscle, the phrenic nerve courses inferiorly through the neck and thorax before reaching its end point, the diaphragm. Thus, the phrenic nerve has a relatively long course before reaching its final destination. Any process that disrupts the transmission of neurologic impulses through the phrenic nerve directly affects the diaphragm. Another eMedicine article, Diaphragm Paralysis, may be of interest.
Pathophysiology
Disorders of innervation During normal respiration, the brain stem sends action potentials to the third through fifth spinal levels, which then give off dorsal rami that convalesce to form the phrenic nerves bilaterally. The phrenic nerves then traverse the neck and thorax and innervate the diaphragm. The successful impulse of respiratory stimulus from the brain to the diaphragm can be compromised by an interruption of the phrenic nerve at any point along this course. Traumatic injury to the head or brain stem prevents nerve signals from reaching the phrenic nerve. Generally, injuries that affect the brain and brain stem are catastrophic, with the chance of survival being grim. Injuries or disease processes that affect the respiratory nervous impulse along its long course are widely described. A number of distinct entities, including trauma, spinal cord disorders, syringomyelia, poliomyelitis, and different motor neuron diseases, decrease the impulse of stimuli to the cervical spinal cord. Peripheral phrenic nerve injuries result from damage to the nerve along its path in the cervical area or the thorax. A number of clinical entities can affect the phrenic nerve directly, including trauma, open heart surgery or thoracic surgery, chiropractic cervical spine manipulation, radiation therapy, demyelinating diseases (eg, Guillain-Barr syndrome), neoplasm, uremia, lead neuropathy, postinfectious neuropathies, and many other processes. Disorders of anatomy Anatomic disorders of the diaphragm are typically classified into 2 broad categories: congenital and acquired. Congenital diaphragmatic hernias occur when the muscular entities of the diaphragm do not develop normally, usually resulting in displacement of abdominal components into the thorax.2 The most common cause of acquired diaphragmatic disorders is trauma3, 4; however, consider several other important entities when observing anatomic defects of the diaphragm in adults. Bochdalek hernias represent the majority of congenital diaphragmatic hernias. The major defects in Bochdalek hernias are posterolateral defects of the diaphragm, which result in either failure in the development of the pleuroperitoneal folds or improper or absent migration of the diaphragmatic musculature.5, 6 Animal models suggest that one potential cause of congenital diaphragmatic hernias is abnormalities of the retinoid system that may result from maternal vitamin A deficiency.7 Patients with congenital diaphragmatic hernias generally present in the neonatal period and have a mortality rate of 45-50%. The morbidity and mortality associated with congenital diaphragmatic hernias relate mostly to hypoplasia of the lung on the affected side. Thus, timely diagnosis and proper management remain the key ingredients to survival.
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Traumatic diaphragmatic rupture can occur secondary to both blunt and penetrating trauma. The prevalence of diaphragmatic rupture is 0.8-1.6% in patients admitted to the hospital for blunt trauma. The major etiologies of diaphragmatic rupture are motor vehicle accidents and penetrating trauma from gunshot and stab wounds. Several theories have been postulated regarding the mechanism of rupture for blunt trauma, including shearing of a stretched membrane, avulsion of the diaphragm from its points of attachment, and sudden force transmission through viscera acting as a viscous fluid. Left-sided rupture is more common than right-sided rupture (68.5% vs 24.2%) because of both hepatic protection and the increased strength of the right hemidiaphragm. However, increased left-sided hernias may also result from weaknesses in points of diaphragmatic embryologic fusion.
Frequency
United States
The exact frequency of many diaphragmatic disorders is not known. The incidence of diaphragmatic dysfunction due to specific etiologies is known. For example, postcardiac surgery diaphragmatic dysfunction is reported in 11% of patients.
Mortality/Morbidity
Morbidity and mortality resulting from diaphragmatic disorders are associated with the etiology of the dysfunction. Individuals with anatomic defects are much more likely to survive than individuals with unresolved defective or absent neurologic impulses. Persons with unilateral dysfunction are much more likely to remain asymptomatic compared with individuals with bilateral involvement.
Patients with neurologic involvement generally recover if dysfunction is not due to a neuropathic process. Phrenic nerve injury during coronary artery bypass surgery is a good example. Recovery may take up to 2 years or longer. Patients with anatomic defects generally do well once the defect is repaired. The outcome of neonates with congenital diaphragmatic hernias generally relates to the pulmonary development after repair of the diaphragmatic defect. Patients with congenital diaphragmatic hernias generally present in the neonatal period and have a mortality rate of 45-50%. The morbidity and mortality associated with congenital diaphragmatic hernias relate mostly to hypoplasia of the lung on the affected side. Thus, timely diagnosis and proper management remain the key ingredients to survival.
Clinical
History
Background information is of prime importance when considering dysfunction of the diaphragm. An adequate history is essential to help identify potential causes. Even so, an etiology for diaphragmatic dysfunction is not ascertained in 50-60% of patients.
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Congenital hernias Respiratory distress and/or cyanosis may occur within the first 24 hours of life. If the defect is small enough, patients often remain asymptomatic for years or even decades. Traumatic rupture The acute phase manifests with abdominal pain, concurrent intra-abdominal and intrathoracic injuries, respiratory distress, and cardiac dysfunction. Latent-phase symptoms include upper GI complaints, pain in the left-upper quadrant or chest, pain in the left shoulder, dyspnea, and orthopnea. The GI obstructive phase manifests with nausea and vomiting with unrelenting abdominal pain, prostration, and respiratory distress. Neurologic causes Most patients with unilateral paralysis are asymptomatic. Manifestations include mild exertional dyspnea, generalized muscle fatigue, chest wall pain, and resting dyspnea while lying with the paralyzed side down. Symptoms are generally more severe in patients with concomitant lung disease. Bilateral paralysis manifests with shortness of breath, severe exertional dyspnea, and marked orthopnea.8 The orthopnea of bilateral diaphragmatic paralysis is dramatic and occurs within minutes after assuming the recumbent position. Orthopnea is associated with tachypnea and rapid, shallow breathing. Patients have a poor quality of sleep, which may cause fatigue. Significant orthopnea sometimes triggers a cardiac workup.
Physical
Physical findings upon examination vary depending on the etiology.
Congenital hernias Right-sided heart Decreased breath sounds on affected side Scaphoid abdomen Auscultation of bowel sounds in the thorax Traumatic rupture Marked respiratory distress Decreased breath sounds on affected side Palpation of abdominal contents in the chest upon insertion of chest tube Auscultation of bowel sounds in chest Paradoxical movement of abdomen with breathing
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Neurologic causes Decreased breath sounds Generalized or focal neurologic deficits Dullness on lower chest upon percussion on the involved side Excursion of involved hemithorax decreased compared with healthy side Paralysis Paradoxical abdominal wall retraction during inspiration (best appreciated on supine position) Hypoxemia, secondary to atelectasis-induced ventilation-perfusion mismatch, exacerbated in supine position Signs of cor pulmonale occasionally present
Causes
The etiology of diaphragmatic dysfunction is most easily separated into anatomic or neurologic causes.
Anatomic defects Congenital defects - Bochdalek hernia, Morgagni hernia, eventration of the diaphragm, and diaphragmatic agenesis Acquired defects - Traumatic rupture, penetrating injuries, idiopathic etiologies, and iatrogenic responses to surgery or other invasive procedures Innervation defects Brain stem stroke Spinal cord disorders - Trauma to the cervical spinal cord, syringomyelia, poliomyelitis, anterior horn cell disease, amyotrophic lateral sclerosis, and motor neuron disease Phrenic nerve neuropathy9 - Trauma to the phrenic nerve from surgery,10 radiation,11 or tumor; Guillain-Barr syndrome; diabetic, nutritional, and alcoholic neuropathy; vasculitic neuropathy; lead and poison neuropathy; and infection-related nerve injury (eg, diphtheria, tetanus, typhoid, measles, botulism) Myasthenia gravis Muscular disorders - Myotonic dystrophies, Duchenne muscular dystrophy, and metabolic myopathies Idiopathic etiologies Postpolio syndrome presenting as isolated diaphragmatic paralysis Phrenic nerve injury due to cold cardioplegia during cardiac surgery10 Thyroid disorders Postviral neuropathy
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Connective-tissue disease (eg, systemic lupus erythematosus, rheumatoid arthritis) - Can lead to progressive shrinking lung syndrome Acid maltase deficiency Malnutrition12 Neurologic causes of diaphragmatic paralysis Spinal cord transaction13 Multiple sclerosis Amyotrophic lateral sclerosis Cervical spondylosis Poliomyelitis Guillain-Barr syndrome Phrenic nerve dysfunction Compression by tumor Cardiac surgery cold injury10 Blunt trauma14, 15 Idiopathic phrenic neuropathy Postviral phrenic neuropathy Radiation therapy11 Cervical chiropractic manipulation16 Myopathic causes of diaphragmatic paralysis Limb-girdle dystrophy Hyperthyroidism or hypothyroidism Malnutrition Acid maltase deficiency Connective-tissue diseases Systemic lupus erythematosus Dermatomyositis Mixed connective-tissue disease Amyloidosis
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Infection Herpes zoster Idiopathic myopathy
Differential Diagnoses
Decreased pulmonary or abdominal compliance Pleural adhesions
Other Problems to Be Considered

Fractures, Cervical Spine Guillain-Barr Syndrome Myasthenia Gravis Cervical fracture Cerebral hemorrhage or ischemia Numerous neuropathies Injury to phrenic nerve from trauma Injury to phrenic nerve from neoplasm Injury to phrenic nerve from surgery (most commonly from cardiac surgery due to cold cardioplegia) Alveolar hypoventilation caused by brainstem or higher cervical spinal injury17 Anterior horn cell or neuromuscular junction disease to differentiate from phrenic nerve dysfunction
Workup
Laboratory Studies
Laboratory studies are limited to discovery of neuropathic causes of diaphragmatic dysfunction. Arterial blood gas determinations may show hypoxemia with underlying V/Q mismatch and progressive hypercapnia as respiratory failure develops.
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Imaging Studies
Chest radiography18 Neurologic impairment manifests radiographically with elevation of the diaphragm (unilateral or bilateral), mediastinal shift upon inspiration, and diminished, absent, or paradoxic movements upon inspiration. Chest radiographs may exhibit a cervical or thoracic mass that encompasses the phrenic nerve. Small lung volume and atelectasis are also common features. Congenital defect or traumatic rupture is demonstrated roentgenographically with abdominal contents in the thorax on the affected side. A nasogastric tube that radiographically appears to be in the thorax may be misinterpreted as a massive hemothorax. Thus, palpation of lung parenchyma and/or abdominal viscus within the thorax before inserting a chest tube into a patient with trauma is always important. Fluoroscopy18 Up to 6% of the healthy population has paradoxic movement of a hemidiaphragm on a deep inspiratory effort against a closed airway (sniff test) as a normal finding. The sniff test result is considered positive if a 2-cm or greater excursion is present and the whole leaf of the hemidiaphragm, in the oblique view, is involved. Fluoroscopy is positive in 90% of cases of unilateral diaphragmatic paralysis. In bilateral paralysis, the sniff test result may be misleading because the cephalad movement of the ribs and accessory muscle contraction gives the false appearance of caudal displacement of the diaphragm. Measurement of diaphragmatic thickness by ultrasonography has been used in a small series to confirm and assess recovery of diaphragmatic paralysis.19 CT scanning is usually not very helpful in bilateral paralysis. Dynamic MRI, however, may prove to be useful.
Other Tests
Pulmonary function tests, including maximum inspiratory pressures, transdiaphragmatic pressure measurement, and vital capacity (VC), in both upright and supine positions, help the clinician determine whether diaphragmatic dysfunction is present and/or the degree of respiratory compromise experienced by the patient in different positions. Significant restrictive physiology is noted in patients with diaphragmatic paralysis. In healthy individuals, a 10% decrease in VC in the supine position typically is present. This decrease in VC may increase to as much as 50% in patients with bilateral diaphragmatic paralysis. In unilateral paralysis, VC decreases by 15-20% in the supine position, but still ranges from 70-80% of predicted. Maximal inspiratory pressure (PI-max) is also a useful test. In patients with systemic or generalized neuromuscular disease and bilateral diaphragmatic paralysis, the PI-max is less than - 60 cm water. In patients with unilateral diaphragmatic paralysis, the PI-max is less useful because it decreases to a value of 60% predicted. Phrenic nerve conduction studies are used to assess the latency of conducting nervous impulses along the course of the nerve. This helps localize lesions to one side or the other and helps the clinician to decipher whether the condition is a bilateral phenomenon. This test is not generally available and may require referral to a center that is able to provide this service. An electromyogram is useful to show neuropathic or myopathic patterns, and the test can be complemented by phrenic nerve stimulation at the neck.20 Magnetometers or inductance plethysmographic coils placed around the abdomen and chest may also provide diagnostic clues by revealing paradoxical chest wall motion.
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Measurement of transdiaphragmatic pressure is the criterion standard in the diagnosis of diaphragmatic dysfunction and paralysis. It reflects the difference between intragastric pressure versus intrapleural pressure. Although this test is effort dependent, the sensitivity can be increased my measuring pressure by electrically stimulating the phrenic nerve and measuring twitch or tetanic transdiaphragmatic pressure. Electromyography has a limited role in unilateral diaphragmatic paralysis. The maximum transdiaphragmatic pressure during static effort is also decreased. M-mode ultrasonography is the latest method to evaluate a paralyzed diaphragm, from which the paralyzed hemidiaphragm shows no active caudal movement with inspiration. MRI of the neck may be useful to determine if the presence of pathologic conditions involving the spinal column and nerve roots are causing diaphragmatic paralysis.
Treatment
Medical Care
Patients with unilateral diaphragmatic paralysis are typically asymptomatic and do not need treatment. Patients may have some dyspnea in physiological situations associated with exertion or if they have an underlying pulmonary disease. Treatment should be considered when dyspnea is out of proportion to the physical exertion. Medical care should be focused on the etiology of the dysfunction. In anatomic causes and defects, the only treatment option is surgical repair. Once an anatomic etiology is considered, the most important next step is to discover the cause. Neurologic processes, depending on the etiology, can generally be treated medically.
Supportive management Many patients with severe diaphragmatic dysfunction require ventilatory support. Depending on the etiology of the disease, some patients only require short-term support, while others may require life-long ventilatory breathing. Most patients with bilateral diaphragmatic paralysis eventually develop progressive ventilatory failure resulting from fatigue of the accessory muscles. Patients may have progressive disease with carbon dioxide retention and irreversible ventilatory failure. These patients require ventilatory assistance. In one study, improvement was demonstrated after ventilatory support with external negative-pressure respirators in patients with overt carbon dioxide retention and decreased central ventilatory drive. Some patients who have decreased ventilatory strength as measured by PI-max and transdiaphragmatic pressures had these measures of respiratory function normalize after a period of negative-pressure ventilatory assistance. Patients with cor pulmonale also may manifest improvement in function and correction of blood gas abnormalities with nighttime or intermittent daytime noninvasive ventilation.21 If the patient does not respond to nasal or oral positive-pressure ventilation, alternative forms of therapy such as negative-pressure cuirass or pulmo-wrap, rocking bed, or positive-pressure pulmo-belt can be used. Tracheotomy with positive-pressure intermittent or permanent ventilation is reserved for patients with life-threatening disease. Patients should undergo a sleep study if he or she is considered for negative-pressure ventilation because it can precipitate or exacerbate preexisting upper airway
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obstruction. Positive-pressure ventilation can minimize the need for a sleep study. If the phrenic nerve is intact and the problem lies in actually transmitting an impulse to the nerve, phrenic nerve or diaphragmatic pacing may be useful modalities in the treatment of this subset of patients.22 Progressive reconditioning is recommended when using a diaphragmatic pacer. High stimulating frequencies and a prolonged period of pacing may lead to irreversible muscle dysfunction. Patients with diaphragmatic pacing require tracheotomies because pacer-induced breathing is not synchronized with the upper airway. Investigations with diaphragmatic pacers and upper airway sensors are ongoing.23, 24 Neurologic Once a diagnosis of neurologic dysfunction is made, ordering studies to determine the cause is vital. A number of neurologic etiologies can be managed medically, but discovering the cause often becomes a challenge.
Surgical Care
Surgery in indicated in the management of anatomic defects in the diaphragm. The type of surgical intervention depends on the anatomic defect or problem.
Congenital defects: Manage congenital diaphragmatic defects through transabdominal primary surgical repair. Acquired defects Manage acquired diaphragmatic defects (ie, traumatic rupture, late-onset congenital diaphragmatic defect) by thoracoscopic plication of the hemidiaphragm. Plication results in improved lung function, exercise endurance, and dyspnea. Plication of the diseased diaphragm improves ventilation to the well-perfused lung and improves gas exchange, which improves static lung mechanics. In a selected group of patients, plication of the diaphragm improved VC by 10-20% and improved PaO2 by 10%.25 A surgical series reported improvement in forced tidal volume from 216 mm/GHz to 415 mm/GHz postplication, and mechanical ventilatory support could be discontinued 2-12 days after plication. Plication can also be achieved by video-assisted thoracoscopy.26 Phrenic nerve injury Primary repair of phrenic nerve damage from trauma can be attempted but does not generally restore function. With expectant treatment, few patients regain phrenic nerve function. Manage injury from a tumor by resection of the tumor encasing the phrenic nerve. Most patients regain function of the nerve. Cold phrenic nerve injury during cardiac surgery generally resolves with expectant management. Spinal cord injury or phrenic nerve injury: Diaphragmatic pacing is a technology that allows the placement electrodes within the diaphragm that stimulate the diaphragm to contract. This can be performed either transthoracically or transabdominally. The more recent studies support the use of laparoscopy and thoracoscopy.
Medication
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Medication is limited to the etiology of neurologic involvement.
Follow-up
Further Outpatient Care
Once an anatomic defect is corrected, the patient should undergo periodic chest radiography and assessment of pulmonary function. Although the rate of spontaneous recurrence of a repaired diaphragmatic hernia is low, small defects in the repair site have been reported. Therefore, surveillance is important. If dysfunction was secondary to a tumor encroaching on the phrenic nerve, maintaining close follow-up contact with the patient is important to ensure that the neoplasm has not recurred.
Complications
Anatomic defects may lead to respiratory failure, incarceration or strangulation of bowel, or hypoplasia of the lung in congenital defects. Neurologic problems may lead to respiratory failure.
Prognosis
Patients with anatomic repairs The prognosis for patients with anatomic repairs from traumatic rupture directly correlates with the extent of concomitant injuries. Neonates generally have a good prognosis after repair of congenital diaphragmatic hernias, but the prognosis is directly related to the development of the lung on the affected side. Patients with neurologic conditions The prognosis for patients with neurologic conditions generally correlates with etiology. Persons with high cervical spine fractures generally fare worse than individuals with transient neuropathies such as Guillain-Barr syndrome. Idiopathic diaphragmatic disease has a variable prognosis, with some patients recovering spontaneously.
Miscellaneous
Medicolegal Pitfalls
Failure to conduct periodic chest radiography and assessment of pulmonary function once an anatomic defect is corrected Failure to maintain close follow-up contact if dysfunction was secondary to a tumor encroaching on the phrenic nerve
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In patients with bilateral diaphragmatic dysfunction, failing to recognize the diagnosis until the patient presents with cor pulmonale and/or cardiorespiratory failure
Multimedia
Media file 1: Radiograph of a man who fell 45 ft from scaffolding, through plate glass windows, and onto the ground. Intraoperatively, he had a completely avulsed diaphragm on the left side. The patient subsequently recovered after a 45-day hospital course of treatment.
References
1. Rochester DF. The diaphragm: contractile properties and fatigue. J Clin Invest. May 1985;75(5):1397-402. [Medline]. 2. Wiseman NE, MacPherson RI. "Acquired" congenital diaphragmatic hernia. J Pediatr Surg. Oct 1977;12(5):657-65. [Medline]. 3. Shah R, Sabanathan S, Mearns AJ, Choudhury AK. Traumatic rupture of diaphragm. Ann Thorac Surg. Nov 1995;60(5):1444-9. [Medline]. 4. Sharma OP. Traumatic diaphragmatic rupture: not an uncommon entity--personal experience with collective review of the 1980's. J Trauma. May 1989;29(5):678-82. [Medline]. 5. Grmoljez PF, Lewis JE Jr. Congenital diaphragmatic hernia: Bochdalek type. Am J Surg. Dec 1976;132(6):744-6. [Medline].
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6. Rees JR, Redo SF, Tanner DW. Bochdalek's hernia. A review of twenty-one cases. Am J Surg. Mar 1975;129(3):259-61. [Medline]. 7. Greer JJ, Babiuk RP, Thebaud B. Etiology of congenital diaphragmatic hernia: the retinoid hypothesis. Pediatr Res. May 2003;53(5):726-30. [Medline]. 8. Kumar N, Folger WN, Bolton CF. Dyspnea as the predominant manifestation of bilateral phrenic neuropathy. Mayo Clin Proc. Dec 2004;79(12):1563-5. [Medline]. 9. Zifko U, Auinger M, Albrecht G, Kastenbauer T, Lahrmann H, Grisold W, et al. Phrenic neuropathy in chronic renal failure. Thorax. Jul 1995;50(7):793-4. [Medline]. 10. Efthimiou J, Butler J, Woodham C, Benson MK, Westaby S. Diaphragm paralysis following cardiac surgery: role of phrenic nerve cold injury. Ann Thorac Surg. Oct 1991;52(4):1005-8. [Medline]. 11. Brander PE, Jarvinen V, Lohela P, Salmi T. Bilateral diaphragmatic weakness: a late complication of radiotherapy. Thorax. Sep 1997;52(9):829-31. [Medline]. 12. Murciano D, Rigaud D, Pingleton S, Armengaud MH, Melchior JC, Aubier M. Diaphragmatic function in severely malnourished patients with anorexia nervosa. Effects of renutrition. Am J Respir Crit Care Med. Dec 1994;150(6 Pt 1):1569-74. [Medline]. 13. Lemons VR, Wagner FC Jr. Respiratory complications after cervical spinal cord injury. Spine. Oct 15 1994;19(20):2315-20. [Medline]. 14. Iverson LI, Mittal A, Dugan DJ, Samson PC. Injuries to the phrenic nerve resulting in diaphragmatic paralysis with special reference to stretch trauma. Am J Surg. Aug 1976;132(2):263-9. [Medline]. 15. van Vugt AB, Schoots FJ. Acute diaphragmatic rupture due to blunt trauma: a retrospective analysis. J Trauma. May 1989;29(5):683-6. [Medline]. 16. Heffner JE. Diaphragmatic paralysis following chiropractic manipulation of the cervical spine. Arch Intern Med. Mar 1985;145(3):562-4. [Medline]. 17. Davis J, Goldman M, Loh L, Casson M. Diaphragm function and alveolar hypoventilation. Q J Med. Jan 1976;45(177):87-100. [Medline]. 18. Gierada DS, Slone RM, Fleishman MJ. Imaging evaluation of the diaphragm. Chest Surg Clin N Am. May 1998;8(2):237-80. [Medline]. 19. Summerhill EM, El-Sameed YA, Glidden TJ, McCool FD. Monitoring recovery from diaphragm paralysis with ultrasound. Chest. Mar 2008;133(3):737-43. [Medline]. 20. Bellemare F, Bigland-Ritchie B. Assessment of human diaphragm strength and activation using phrenic nerve stimulation. Respir Physiol. Dec 1984;58(3):263-77. [Medline]. 21. Hill NS. Noninvasive ventilation. Does it work, for whom, and how?. Am Rev Respir Dis. Apr 1993;147(4):1050-5. [Medline]. 22. DiMarco AF, Onders RP, Kowalski KE, Miller ME, Ferek S, Mortimer JT. Phrenic nerve pacing in a tetraplegic patient via intramuscular diaphragm electrodes. Am J Respir Crit Care Med. Dec 15 2002;166(12 Pt 1):1604-6. [Medline]. 23. Glenn WW. The treatment of respiratory paralysis by diaphragm pacing. Ann Thorac Surg. Aug 1980;30(2):106-9. [Medline]. 24. Glenn WW, Hogan JF, Loke JS, Ciesielski TE, Phelps ML, Rowedder R. Ventilatory support by pacing of the conditioned diaphragm in quadriplegia. N Engl J Med. May
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3 1984;310(18):1150-5. [Medline]. 25. Ciccolella DE, Daly BD, Celli BR. Improved diaphragmatic function after surgical plication for unilateral diaphragmatic paralysis. Am Rev Respir Dis. Sep 1992;146(3):797-9. [Medline]. 26. Freeman RK, Wozniak TC, Fitzgerald EB. Functional and physiologic results of video-assisted thoracoscopic diaphragm plication in adult patients with unilateral diaphragm paralysis. Ann Thorac Surg. May 2006;81(5):1853-7; discussion 1857. [Medline]. 27. Alexander C. Diaphragm movements and the diagnosis of diaphragmatic paralysis. Clin Radiol. Jan 1966;17(1):79-83. [Medline]. 28. Baum GL, Crapo JD, Celli BR, eds. Textbook of Pulmonary Diseases. 6th ed. Boston, Mass: Little Brown & Company; 1995. 29. Fell SC. Surgical anatomy of the diaphragm and the phrenic nerve. Chest Surg Clin N Am. May 1998;8(2):281-94. [Medline]. 30. Fitting JW, Grassino A. Diagnosis of diaphragmatic dysfunction. Clin Chest Med. Mar 1987;8(1):91-103. [Medline]. 31. Gibson GJ. Diaphragmatic paresis: pathophysiology, clinical features, and investigation. Thorax. Nov 1989;44(11):960-70. [Medline]. 32. Murray JF, Nadel JA, eds. Textbook of Respiratory Medicine. Philadelphia, Pa: WB Saunders; 1997.
Keywords
diaphragm disorders, diaphragm dysfunction, phrenic nerve injury, diaphragm, respiratory dysfunction, Bochdalek hernias, congenital diaphragmatic hernia, Guillain-Barr syndrome, lead neuropathy, postinfectious neuropathies, chiropractic cervical spine manipulation, uremia, diaphragmatic rupture, Morgagni hernia, eventration of the diaphragm, diaphragmatic agenesis, syringomyelia, poliomyelitis, motor neuron disease, brachial plexus neuritis, diabetic neuropathy, nutritional neuropathy, alcoholic neuropathy, vasculitic neuropathy, infection-related nerve injury, myasthenia gravis, myotonic dystrophies, Duchenne muscular dystrophy, metabolic myopathies, polymyositis, acquired diaphragmatic disorders, innervation defects, cerebral stroke, spinal cord disorders, phrenic nerve neuropathy
Contributor Information and Disclosures

Author
Abhijit A Raval, MD, Pulmonary Diseases and Critical Care Fellow, James H Quillen College of Medicine Disclosure: Nothing to disclose
Coauthor
Ryland P Byrd Jr, MD, Professor, Department of Internal Medicine, Division of Pulmonary Medicine and Critical Care Medicine, James H Quillen College of Medicine, East Tennessee State University; Chief of Pulmonary Medicine, Medical Director of Respiratory Therapy, Intensive Care Unit, Program Director of Pulmonary Diseases and Critical Care Medicine Fellowship, James H Quillen Veterans Affairs Medical Center Ryland P Byrd Jr, MD is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society, and Southern Medical Association
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Disclosure: Nothing to disclose

Medical Editor
Ryland P Byrd Jr, MD, Professor, Department of Internal Medicine, Division of Pulmonary Medicine and Critical Care Medicine, James H Quillen College of Medicine, East Tennessee State University; Chief of Pulmonary Medicine, Medical Director of Respiratory Therapy, Intensive Care Unit, Program Director of Pulmonary Diseases and Critical Care Medicine Fellowship, James H Quillen Veterans Affairs Medical Center Ryland P Byrd Jr, MD is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society, and Southern Medical Association Disclosure: Nothing to disclose
Pharmacy Editor
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine Disclosure: Nothing to disclose
Managing Editor
Om Prakash Sharma, MD, FRCP, FCCP, DTM&H, Professor, Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of Southern California Keck School of Medicine Om Prakash Sharma, MD, FRCP, FCCP, DTM&H is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Osler Society, American Thoracic Society, New York Academy of Medicine, and Royal Society of Medicine Disclosure: Keck School of Medicine, USC None
CME Editor
Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians Disclosure: Nothing to disclose
Chief Editor
Zab Mosenifar, MD, Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center; Professor of Medicine, David Geffen School of Medicine at UCLA Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society Disclosure: Nothing to disclose
Acknowledgments The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors, Anne T. Saladyga, MD, Jason M. Johnson, DO, and Sidney R. Steinberg, MD, FACS, to the development and writing of this article. 1994-2009 by Medscape.
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Diaphragm Disorders - (Print..

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Diaphragm Disorders: [Print] - eMedicine Pulmonology