Unilateral Diaphragmatic Paralysis Research Articles

Diaphragmatic paralysis: the use of M mode ultrasound for diagnosis in adults

Retrospective, case series. To evaluate the use of M mode ultrasonography in the evaluation of diaphragmatic paralysis in adults. Radiology department, Princess Alexandra Hospital, Brisbane, Australia. Ten patients who were referred for evaluation of suspected diaphragmatic paralysis were evaluated using M mode ultrasound. Three of the patients who were scanned demonstrated normal diaphragmatic movement. The M mode trace demonstrated normal movement of the diaphragm bilaterally with quiet respiration and a sharp upstroke on the sniff test (indicating normal caudal movement of the diaphragm). Six patients were found to have a unilateral diaphragmatic paralysis. Four of these patients were noted to have a raised hemi-diaphragm on chest radiography. Of the two who did not have a raised hemi-diaphragm on chest radiography, one was permanently ventilated. The M mode trace of the paralyzed side showed no active caudal movement of the diaphragm with inspiration and abnormal paradoxical movement (ie cranial movement on inspiration) particularly with the sniff test. M mode ultrasonography is a relatively simple and accurate test for diagnosing paralysis of the diaphragm, in the adult population. It can be performed, if necessary, at the bedside and can be easily repeated if paralysis is not thought to be permanent. Philips ATL Sono CT 5000 using a 2-5 MHz curved linear transducer.

SLEEP-RELATED DESATURATION IN PATIENTS WITH UNILATERAL DIAPHRAGMATIC DYSFUNCTION

PURPOSE: Benign unilateral diaphragmatic dysfunction or paralysis (BUDDP) is not associated with known malignancy and may be idiopathic or due to previous trauma. BUDDP is generally thought to be of little clinical significance. Previous studies have been of limited scope, and have not included sleep studies. We assessed the physiologic and polysomnographic findings in 6 patients with BUDDP.

Pulmonary function after complete unilateral phrenic nerve transection

The status of pulmonary function following phrenic nerve transfer surgery is still largely unknown because of the high degree of variability in the accessory phrenic nerve that may be involved. In the present study, pulmonary functions were assessed in patients before and after full-length phrenic nerve transfer surgery, in whom the phrenic nerve was severed at a location just before its entry into the diaphragm. Fifteen patients (average age 27.4 years) with complete brachial plexus palsy underwent full-length phrenic nerve transfer. The phrenic nerve was harvested from the thoracic cavity by means of video-assisted thoracic surgery and then transferred to the musculocutaneous nerve. Postoperative pulmonary functions were retrospectively analyzed. Patients underwent follow-up evaluation for 42 to 48 months; four patients were eventually lost to follow up. Although no patient experienced pulmonary problems following the surgery, all sustained varying degrees of diaphragmatic paralysis and elevation (for 1-1.5 intercostal spaces) on the surgically treated side as seen on chest x-ray films. Pulmonary functional parameters, including vital capacity, vital capacity in percentage of predicted values, residual volume, total lung capacity, forced vital capacity, and forced expiratory volume in 1 second, recovered to preoperative levels by 1 year postsurgery. In contrast, the postoperative maximal inspiratory pressure value was significantly decreased compared with the predicted values (average decrease approximately 20%) in all of the patients, even at 4 years after the surgery. In young patients with healthy lung function, unilateral phrenic nerve transection surgery can cause unilateral diaphragmatic paralysis and reduce the inspiration muscle force; however, most pulmonary function parameters gradually recover to preoperative levels within 1 year.

Unilateral paralysis of the diaphragm during pregnancy: Case report and literature review

Unilateral diaphragmatic paralysis is usually asymptomatic and diagnosed incidentally and often does not need any additional diagnostic workup, but in the setting of pregnancy it may require additional investigations. We describe a patient in her last trimester of pregnancy (36th week) who presented to the hospital with symptoms suggestive of upper respiratory tract infection and with a chest radiograph showing left diaphragmatic eventration, for which she underwent thoracotomy and cesarean section. In the report, we review the normal respiratory changes associated with pregnancy and discuss the management of patients with diaphragmatic paralysis and pregnancy.

Determinants of diaphragm motion in unilateral diaphragmatic paralysis.

Cranial displacement of a hemidiaphragm during sniffs is a cardinal sign of unilateral diaphragmatic paralysis in clinical practice. However, we have recently observed that isolated stimulation of one phrenic nerve in dogs causes the contralateral (inactive) hemidiaphragm to move caudally. In the present study, therefore, we tested the idea that, in unilateral diaphragmatic paralysis, the pattern of inspiratory muscle contraction plays a major role in determining the motion of the inactive hemidiaphragm. We induced a hemidiaphragmatic paralysis in six anesthetized dogs and assessed the contour of the diaphragm during isolated unilateral phrenic nerve stimulation and during spontaneous inspiratory efforts. Whereas the inactive hemidiaphragm moved caudally in the first instance, it moved cranially in the second. The parasternal intercostal muscles were then severed to reduce the contribution of the rib cage muscles to inspiratory efforts and to enhance the force generated by the intact hemidiaphragm. Although the change in pleural pressure (DeltaPpl) was unaltered, the cranial displacement of the paralyzed hemidiaphragm was consistently reduced. A pneumothorax was finally induced to eliminate DeltaPpl during unilateral phrenic nerve stimulation, and this enhanced the caudal displacement of the inactive hemidiaphragm. These observations indicate that, in unilateral diaphragmatic paralysis, the motion of the inactive hemidiaphragm is largely determined by the balance between the force related to DeltaPpl and the force generated by the intact hemidiaphragm.

Effect of unilateral diaphragm paralysis on branch pulmonary artery flow

Background: Respiration is known to be a significant contributor to pulmonary flow in patients who have had Glenn or Fontan procedures. Objective: The purpose of this study was to evaluate the effect of respiration on branch pulmonary artery flow in normal participants, in those with uncomplicated Glenn or Fontan procedures, and in those with uncomplicated biventricular (2V) repairs, and to compare them with similar groups of postoperative patients who had unilateral diaphragm paralysis. Methods: Twenty-one normal infants and children were studied, along with 10 who had undergone uncomplicated bidirectional Glenn or Fontan palliation. Also studied were 10 patients with uncomplicated 2V repairs and 17 patients having ultrasound demonstration of diaphragm paralysis. Nine had undergone Glenn or Fontan procedures and 8 had undergone 2V repair. With the use of conventional pulsed Doppler, branch right and left pulmonary artery waveforms were recorded during spontaneous respiration. The velocity time integral (VTI); heart rate (HR); and systolic, diastolic, and mean velocities were measured at end-expiration and during inspiration. The pulsatility index (PI) (PI = systolic velocity − diastolic velocity/mean velocity) was calculated for each condition. Results: In normal participants PI was 1.69 with a 4.7% increase with inspiration; VTI × HR was 1859. In patients who had undergone uncomplicated Glenn/Fontan procedures PI was 1.06 with a 27.5% increase with inspiration; VTI × HR was 1303, all P = .001 versus normal participants. In patients with 2V repairs PI was 1.7 with a 5.6% increase with inspiration; VTI × HR was 1850, all P = ns versus normal participants. Patients with Glenn/Fontan connections and diaphragm paralysis had lower PI (0.81), inspiratory increase (7.9%), and VTI × HR (610) on the affected side, all P = .001 versus the normal side, and versus patients who had undergone uncomplicated Glenn/Fontan procedures. Patients with 2V repair with a pulsatile source of pulmonary flow had a smaller significant difference in the measured indices. Three patients underwent diaphragm plication with improvement in PI, inspiratory increase in PI, and VTI × HR postplication. Conclusion: In normal participants and patients with uncomplicated 2V repair, inspiration has little effect on PI in branch pulmonary arteries. In patients who have undergone uncomplicated Glenn/Fontan procedures, PI is less than that of normal participants and the effect of inspiration is approximately 5-fold greater. This significant effect of inspiration on pulmonary flow is lost on the affected side in patients with Glenn/Fontan connections and diaphragm paralysis, and is blunted on the affected side in patients with 2V repair and diaphragm paralysis. Loss of diaphragm function is associated with redistribution of pulmonary flow away from the affected side. (J Am Soc Echocardiogr 2002;15:1132-9.)

Effect of severe isolated unilateral and bilateral diaphragm weakness on exercise performance.

Patients with isolated diaphragm paralysis depend on recruitment of extradiaphragmatic respiratory muscles to increase ventilation, but little is known about exercise performance or the response of the inspiratory muscles to loaded breathing. By convention, unilateral diaphragm paralysis is regarded as a trivial condition whereas bilateral paralysis is considered to be potentially life-threatening. In fact, no data exist concerning exercise performance under these conditions. We studied incremental treadmill exercise performed by eight patients with bilateral diaphragm paralysis, eight patients with unilateral diaphragm paralysis, and eight age-matched control subjects. Respiratory muscle endurance (RME) was also measured by an inspiratory threshold loading method. Exercise time, compared with control subjects (671 seconds), was moderately reduced in unilateral diaphragm paralysis (512 seconds, p = 0.07) and further reduced in bilateral diaphragm paralysis (456 seconds, p = 0.02). Similarly, peak minute ventilation was lower in patients with unilateral diaphragm paralysis (84 L x min(-1), p = 0.01) and in patients with bilateral diaphragm paralysis (69 L x min(-1), p = 0.001) compared with control subjects (114 L x min(-1)). However, patients with unilateral diaphragm paralysis and patients with bilateral diaphragm paralysis had increased ratios of peak oxygen consumption to peak minute ventilation compared with control subjects (p = 0.0007 and p < 0.0001, respectively). Nine patients had normal RME; exercise time was moderately increased in these patients (502 seconds) compared with seven patients with reduced RME (461 seconds). In conclusion, although exercise performance is impaired in bilateral diaphragm paralysis, these patients can sustain a reasonable exercise load, particularly if RME is preserved and compensatory mechanisms have developed. In addition, exercise tolerance is diminished in patients with unilateral diaphragm paralysis.

Long term results of diaphragmatic plication for unilateral diaphragm paralysis.

To examine whether diaphragmatic plication is an effective and lasting treatment option for non-malignant diaphragmatic paralysis. Nineteen patients who had undergone diaphragm plication (1983-1990) were recalled for interview, pulmonary function testing and chest X-ray. There were 13 men and six women aged 24-73 (mean 55). Diaphragm paralysis was idiopathic (n=9), postsurgical (n=3), related to cervical spondylosis (n=4) and neck injury (n=2). Patients presented with breathlessness (18/19) or orthopnoea (1/19). Symptoms had lasted 3-60 months (mean 24 months). All patients had a raised hemidiaphragm on chest X-ray with paradoxical movement on ultrasound. Mean preoperative FVC was 71% predicted (range 38-93, SD 12.9) and mean FEV(1) was 67% predicted (range 33-90, SD 10.8). Supine lung volumes were 81% (mean) of sitting values. There were six right plications and 13 left. There were no postoperative deaths. One patient required re-plication. Follow-up (18/19 of original operated patients) ranged from 7-14 years (mean 10 years). Three patients had died of unrelated causes and one patient failed to attend long term follow-up, leaving 15 patients of the original 19 operated on. Positional change in lung volumes was not affected by surgery at early (6 week) or late (>5 year) follow-up. FVC, FEV(1), FRC and TLC improved by 10.1*, 11.8*, 16.9* and 9.2*%, respectively, at early follow-up and 11.8*, 15.4*, 26 and 13.3*% at late follow-up (*P<0.005 signed rank). Dyspnoea scores at long term follow-up improved 1 point (n=5), 2 points (n=5) and 3 points (n=2), remained unchanged (n=1) or dropped 1 point (n=2). Of the 15 patients followed up all but one who had been employed returned to work. 14/15 patients expressed satisfaction with their surgery. Diaphragm plication is an effective procedure with lasting results.

Respiratory Management of Diaphragm Paralysis

The diaphragm is the most important muscle of ventilation. Its contraction is key to the development of intrathoracic pressures. Diseases that affect diaphragmatic function result in decreased pressure-generating capacity by the respiratory muscles. If the involvement is severe or if there is underlying respiratory pathology, diaphragmatic paralysis can lead to overt ventilatory failure. Diaphragmatic involvement can occur unilaterally or bilaterally from systemic diseases or from diseases primarily affecting the diaphragm. Whatever the cause, unilateral diaphragmatic paralysis is usually well tolerated if there is no underlying lung or ribcage pathology. However, under conditions of increased loads, unilateral diaphragmatic paralysis can cause dyspnea and hypoxemia and require treatment. Bilateral diaphragmatic paralysis of any etiology is usually symptomatic and may result in ventilatory failure when severe, or when associated with underlying lung pathology. In some patients unilateral or bilateral paralysis can improve spontaneously but usually over prolonged periods of time. In patients with significant symptoms or development of ventilatory failure, symptoms and outcomes are improved by treatment with noninvasive ventilation or, in selected cases of unilateral paralysis, surgical plication of the diaphragm.

Parálisis diafragmática unilateral tratada con éxito mediante plicatura diafragmática

Unilateral diaphragmatic paralysis is rare and usually due to interrupted phrenic nerve conduction of impulses. The idiopathic form is the most common and viral infection has been suggested as the cause. Generally, clinical repercussions are few but may be severe in some cases. We report a case of unilateral diaphragmatic paralysis that was successfully treated by plication of the diaphragm affected.

Unilateral Diaphragmatic Paralysis Following Bronchial Artery Embolization for Hemoptysis

Bronchial artery embolization is an effective treatment for patients with hemoptysis. Serious complications are rare, but may occur if the arterial supply to other structures is compromised. We present a case of unilateral diaphragmatic paralysis following bronchial artery embolization in a patient with cystic fibrosis. We believe that the diaphragmatic paralysis was due to the inadvertent obstruction of the left pericardiacophrenic artery during the embolization procedure, with compromise of the phrenic nerve blood supply. This resulted in a significant loss of lung function in our patient, who did not recover despite the subsequent return of diaphragmatic function.

Thoracoscopic plication of diaphragmatic eventration using endostaplers

Unilateral diaphragmatic eventration and paralysis require plication in cases of progressive dyspnea on exertion and recurrent respiratory infection. The patient, a 40-year-old woman, who had complained of worsening dyspnea on exertion and elevation of the left diaphragm on chest radiographs for 4 years, underwent plication by thoracoscopy with knifeless endostaplers. Improvements in pulmonary functions and dyspnea on exertion have been maintained for 14 months.

Mediastinitis esclerosante crónica: una causa infrecuente de parálisis diafragmática unilateral

Chronic sclerosing mediastinitis (CSM) is a rare disease whose etiology varies and which usually develops through mediastinal compression syndromes, generally due to occlusion of the superior vena cava. We report a case of CSM diagnosed after a chance finding of unilateral diaphragm paralysis, a circumstance not previously reported in the literature. We review the clinical, radiological and histological features of CSM.

Assessment of diaphragm paralysis with oesophageal electromyography and unilateral magnetic phrenic nerve stimulation.

The purpose of this study was to establish a sensitive and reliable method of diagnosing diaphragm paralysis by recording the diaphragm compound muscle action potential (CMAP) using a multipair oesophageal electrode and unilateral magnetic phrenic nerve stimulation. An oesophageal electrode catheter was designed containing six coils (1 cm wide and 3 cm apart), creating an array of four sequential electrode pairs. The oesophageal catheter was taped at the nose with the proximal electrode pair 40 cm from the nares. Eight patients with unilateral (n=5) or bilateral (n=3) diaphragm paralysis were studied. Five to seven phrenic nerve stimulations were performed at 80% of maximum magnetic stimulator output and the CMAPs were recorded simultaneously from the four pairs of electrodes. In the five patients with unilateral diaphragm paralysis, the CMAP amplitudes and latencies were 1.16+/-0.29 mV and 7.6+/-1.5 ms for functioning sides. No diaphragm CMAP could be detected when stimulating nonfunctioning phrenic nerves. This study shows that diaphragm paralysis can be reliably diagnosed by unilateral magnetic stimulation combined with a multipaired oesophageal electrode.

Mediastinal neurofibroma as a cause of unilateral diaphragm paralysis in von Recklinghausen's disease

Mediastinal neurofibroma as a cause of unilateral diaphragm paralysis in von Recklinghausen's disease

Selective resection of the phrenic nerve roots in rabbits: Part I: Cartography of the residual innervation

Partial unilateral diaphragmatic paralysis remains poorly understood. This study evaluates the residual innervation of the diaphragm after selective resection of one or several roots of the right phrenic nerve in rabbits. Forty-seven animals were operated on according to five root resection modalities. Seven animals served as control. Eight weeks after surgery, the different regions of each hemidiaphragm were analyzed. Electromyographic activity was measured during quiet inspiration and the following histomorphometric parameters were studied: mean fiber area, fiber area dispersion, and ratio large diameter over small diameter. The results obtained from the two measurements were similar. When the accessory phrenic nerve was spared, the crural diaphragmatic region was preserved; denervation was encountered in anterior and lateral parts of the hemidiaphragm. When the highest root of the right phrenic nerve was resected, denervation was limited to the sternal region. When resection of the two highest roots was performed, partial denervation was observed in each region, with residual innervation in the posterior hemidiaphragm. When resection of both the lowest roots was performed, denervation was maximal in the costal region; sternal region remained intact. No contralateral innervation was observed. We conclude that in rabbits: 1) resection of a single root of the phrenic nerve preserves consistent residual innervation. 2) somatotopy of the diaphragm innervation follows an anteroposterior distribution.

Ultrasound evaluation of the paralyzed diaphragm.

Ultrasound has been used to evaluate diaphragm thickness in the zone of apposition of the diaphragm to the rib cage. The purpose of this study was to determine if ultrasonography could distinguish between a paralyzed and normally functioning diaphragm. We predicted that a paralyzed diaphragm would be atrophic and not shorten, therefore it would be thin and not thicken during inspiration. Thirty subjects (five with bilateral diaphragm paralysis, seven with unilateral diaphragm paralysis, three with inspiratory weakness but normally functioning diaphragms, and 15 healthy control subjects) had diaphragm ultrasound performed with a 7.5 to 10.0 MHz transducer placed over the lower rib cage in the mid-axillary line. The thickness of the diaphragm (tdi) was measured to the nearest 0.1 mm at FRC (t(di)FRC) and TLC (t(di)TLC). Diaphragm thickening during inspiration (delta t(di)) was calculated as (t(di)TLC - t(di)FRC)/t(di)FRC. In patients with unilateral paralysis, t(di) and delta t(di) for the paralyzed hemidiaphragm were significantly less than those values for the normally functioning hemidiaphragm (1.7 +/- 0.2 mm versus 2.7 +/- 0.5 mm [mean + SD] p < 0.01 for t(di), and -8.5 +/- 13% versus 65 +/- 26% [p < 0.001] for delta t(di)). The t(di) and delta t(di) for patients with bilateral diaphragm paralysis were significantly less than those values for the healthy volunteers (1.8 +/- 0.2 versus 2.8 +/- 0.4 and -1 +/- 15% versus 37 +/- 9% for t(di) and delta t(di), respectively) (p < 0.001). We conclude that ultrasound measurements of t(di) and delta t(di) can be used to determine if a diaphragm is paralyzed and confirm our predictions that a chronically paralyzed diaphragm is atrophic and does not thicken during inspiration.

Phrenic nerve injury following scalenectomy in a patient with thoracic outlet obstruction

We present a case in which a patient with normal pulmonary reserve experienced orthopnea and hypoxia secondary to unilateral diaphragmatic paralysis following right scalenectomy. This operation was performed in an attempt to relieve neurovascular compromise at the thoracic outlet. To our knowledge, this association has not been previously described in the literature.

Unilateral Phrenic Nerve Paralysis From Cutting Down a Christmas Tree

Stretch injury to the phrenic nerve is an unusual cause of unilateral diaphragmatic paralysis. In this case the injury occurred while the patient was lying on the ground and cutting down a Christmas tree with a hand saw.

Diaphragmatic dysfunction in neuralgic amyotrophy: an electrophysiologic evaluation of 16 patients presenting with dyspnea.

We report 16 adult men (age, 41 to 75 yr) with neuralgic amyotrophy (NA) who presented with dyspnea due to involvement of the diaphragm. All patients developed breathlessness after a prodrome of acute severe neck and shoulder pain. Bilateral diaphragm paralysis (BDP) was confirmed in 12 patients and unilateral diaphragm paralysis (UDP) in four by the absence of electrical and mechanical responses to percutaneous phrenic nerve stimulation. Global expiratory muscle strength was well preserved in all patients, but inspiratory muscle strength was reduced in proportion to the extent of diaphragmatic involvement. Lung function showed low lung volumes with preservation of carbon monoxide transfer coefficient in all patients. Two BDP patients were hypoxic (PaO2 = 67 and 54 mm Hg, respectively) on daytime arterial blood gas analysis; the latter patient with pre-existing chronic obstructive pulmonary disease and marked obesity also had borderline hypercapnia (PaO2 = 49 mm Hg). Overnight sleep studies in three BDP and two UDP patients showed frequent intermittent arterial oxygen desaturations apparently caused by obstructive sleep apneas, but there was no evidence of alveolar hypoventilation. Follow-up muscle studies in five BDP and four UDP patients between 2 and 4 yr after initial referral showed complete recovery of diaphragmatic function in only two UDP patients, one of whom relapsed a year later. We postulate that NA may be an important but underrecognized cause of diaphragmatic paralysis in otherwise normal patients. Diaphragmatic strength returns very slowly, if at all.