Bilateral Diaphragmatic Paralysis Research Articles

Orthopnea secondary to brachial plexitis with bilateral diaphragmatic paralysis

BackgroundDiaphragmatic paralysis can present with orthopnea. We report a unique presentation of bilateral diaphragmatic paralysis, an uncommon diagnosis secondary to an unusual cause, brachial plexitis. This report thoroughly describes the patient’s presentation, workup, management, and outcome. It also reviews the literature on diaphragmatic paralysis and Parsonage-Turner syndrome.Case presentationA 50-year-old male patient developed insidious orthopnea associated with left shoulder and neck pain over three months with no associated symptoms. On examination, marked dyspnea was observed when the patient was asked to lie down; breath sounds were present and symmetrical, and the neurological examination was normal. The chest radiograph showed an elevated right hemidiaphragm. Echocardiogram was normal. There was a 63% positional reduction in Forced Vital Capacity and maximal inspiratory and expiratory pressures on pulmonary function testing. The electromyogram was consistent with neuromuscular weakness involving both brachial plexus and diaphragmatic muscle (Parsonage and Turner syndrome).ConclusionsCompared to unilateral, bilateral diaphragmatic paralysis may be more challenging to diagnose. On PFT, reduced maximal respiratory pressures, especially the maximal inspiratory pressure, are suggestive. Parsonage-Turner syndrome is rare, usually with unilateral diaphragmatic paralysis, but bilateral cases have been reported.

Quality-of-life impact of diaphragm plication in patients with diaphragmatic paralysis: A retrospective study.

While the overall incidence and prevalence of diaphragmatic paralysis are unknown due to a wide variety of underlying causes, symptomatic patients experience a marked decline in their quality of life. The goal of this study was to measure the impact of diaphragm plication surgery on the quality of life in patients who were diagnosed with diaphragmatic paralysis. A retrospective review of the medical records of 46 patients who underwent diaphragmatic plication surgery was performed. The review included patients who experienced unilateral and bilateral diaphragmatic paralysis. Patients who underwent repeat diaphragm plication surgery were also included in the study. Patients from the retrospective cohort were then contacted by telephone to answer the Dyspnea-12 (D-12) questionnaire. Patients were asked to recall the severity of their symptoms and quality of life preplication, 1-month postplication, and 6-month postplication. Severity of symptoms was ranked as either none, mild, moderate, or severe. Values were then assigned to each rank as follows: none = 0, mild = 1, moderate = 2, and severe = 3. Relative change and statistical significance were calculated with preplication measurements used as the baseline. Scores between preplication versus 1-month postplication and 6-month postplication were then compared by Student's paired t-test. All tests were two-sided and statistical significance was set at P < 0.05. Forty-six patients were included in the study, from which 21 answered the D-12 questionnaire. Average scores from each component of the D-12 questionnaire showed improvement in the severity of symptoms from preplication to 1-month postplication. The latter period was then followed by continued improvement in all areas when symptoms 6-month postplication were assessed. In patients with diaphragmatic paralysis, diaphragm plication was effective in reducing patients' symptoms while improving overall quality of life.

First experience of implantation of diaphragm pacemakers in infant with bilateral diaphragmatic paralysis

First experience of implantation of diaphragm pacemakers in infant with bilateral diaphragmatic paralysis

Hepatitis E virus-associated brachial neuritis presenting with orthopnoea as a result of bilateral diaphragmatic weakness

British Journal of Hospital MedicineVol. 84, No. 2 Case ReportHepatitis E virus-associated brachial neuritis presenting with orthopnoea as a result of bilateral diaphragmatic weaknessSamuel Mackrill, Prithwiraj Chakrabarti, Richard Butterworth, Veeresh PatilSamuel MackrillCorrespondence to: Samuel Mackrill; E-mail Address: [email protected]Department of Medicine, Milton Keynes University Hospital, Milton Keynes, UKSearch for more papers by this author, Prithwiraj ChakrabartiDepartment of Medicine, Milton Keynes University Hospital, Milton Keynes, UKSearch for more papers by this author, Richard ButterworthDepartment of Medicine, Milton Keynes University Hospital, Milton Keynes, UKSearch for more papers by this author, Veeresh PatilDepartment of Medicine, Milton Keynes University Hospital, Milton Keynes, UKSearch for more papers by this authorSamuel Mackrill; Prithwiraj Chakrabarti; Richard Butterworth; Veeresh PatilPublished Online:9 Feb 2023https://doi.org/10.12968/hmed.2022.0280AboutSectionsView articleView Full TextPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareShare onFacebookTwitterLinked InEmail View article References McLean BN, Gulliver J, Dalton HR. Hepatitis E virus and neurological disorders. Pract Neurol. 2017;17(4):282–288. https://doi.org/10.1136/PRACTNEUROL-2016-001588 Crossref, Medline, Google ScholarNoushad MA, Limnatitou D, Bhattacharjee S, Mohd Nor A. Diaphragmatic paralysis resulting in respiratory failure as a feature of hepatitis E virus-associated neuralgic amyotrophy. BMJ Case Rep. 2021;14(4):e242113. https://doi.org/10.1136/BCR-2021-242113 Crossref, Medline, Google ScholarShinder N, Polson A, Pringle E, O'Donnell DE. Neuralgic amyotrophy: a rare cause of bilateral diaphragmatic paralysis. Can Respir J. 1998;5(2):139–142. https://doi.org/10.1155/1998/926375 Crossref, Medline, Google Scholarvan Eijk JJJ, Dalton HR, Ripellino P et al.. Clinical phenotype and outcome of hepatitis E virus-associated neuralgic amyotrophy. Neurology. 2017;89(9):909–917. https://doi.org/10.1212/WNL.0000000000004297 Crossref, Medline, Google Scholar FiguresReferencesRelatedDetails 2 February 2023Volume 84Issue 2ISSN (print): 1750-8460ISSN (online): 1759-7390 Metrics History Published online 9 February 2023 Published in print 2 February 2023 Information© MA Healthcare LimitedPDF download

Bilateral diaphragm paralysis: a clinical case

Diaphragm dysfunction is a rare cause of respiratory distress with a variety of clinical manifestations that complicate diagnosis and treatment. The given clinical case demonstrates the possibility of detecting bilateral diaphragm paralysis using available general clinical and instrumental diagnostic methods. Among the physical data, high standing of the lower borders of the lungs with limited mobility and paradoxical movement of the diaphragm during the Mueller test have a high diagnostic value. Chest X-ray demonstrates the high standing of both domes of the diaphragm and subsegmental atelectasis in the basal parts of the lungs. Severe hypoxemia developed: oxygen saturation in clino- and orthostasis was 72 and 96%, respectively. The tests of pulmonary function showed significant restrictive impairments, a decrease in the vital capacity of the lungs was also determined. Ultrasound examination of the diaphragm revealed hyperechogenicity, lack of inspiratory thickening, and respiratory mobility of the domes of the diaphragm. Electromyography confirmed gross right and left phrenic nerve axonopathy. An idiopathic variant of diaphragm dysfunction can be assumed based on the patient stabilization during CPAP therapy, physiotherapy exercises, chest massage, followed by the disappearance of signs of bilateral diaphragm paralysis. Conclusion. The presented case demonstrates the difficulties of diagnosing bilateral diaphragm paralysis. The final diagnosis was made through the use of specific research methods recommended for suspected diaphragm dysfunction. The prognosis of the idiopathic variant of bilateral diaphragm paralysis, as in this case, is favorable. Spontaneous remission was observed.

Sleep Disordered Breathing Postcoronary Artery Bypass Graft Surgery: A Case Report

Unilateral diaphragmatic paralysis (UDP) is usually found incidentally in those who underwent chest radiography for some other reason. Often patients are asymptomatic at rest but may have breathlessness upon exertion and have a decrease in exercise capacity. Dyspnea at rest may occur if the patient has an underlying lung disease. Few develop orthopnea, which is less intense than patients with bilateral diaphragmatic paralysis (DP). Others present with positional snoring and progressive orthopnea misinterpreted it as sleep-disordered breathing. Here we present a 54-year-old male who presented late with sleep-disordered breathing and was diagnosed to have diaphragmatic palsy postcoronary artery bypass graft.

GASTROESOPHAGEAL REFLUX DISEASE AND PHRENIC NERVE INJURY: A RETROSPECTIVE ANALYSIS OF 518 PATIENTS WITH CLINICALLY SIGNIFICANT DIAPHRAGM PARALYSIS

GASTROESOPHAGEAL REFLUX DISEASE AND PHRENIC NERVE INJURY: A RETROSPECTIVE ANALYSIS OF 518 PATIENTS WITH CLINICALLY SIGNIFICANT DIAPHRAGM PARALYSIS

Atypical Presentation of Mixed Connective Tissue Disorder Involving Bilateral Diaphragm

Pulmonary manifestations can be present in 20-80% of patients having mixed connective tissue disorder (MCTD) and are usually subacute. MCTD when associated with polymyositis can rarely involve the diaphragm, causing respiratory failure.We present herein the case of a 49-year-old female having MCTD with a component of polymyositis who presented with bilateral diaphragmatic paralysis followed by heart failure requiring respiratory support with non-invasive mechanical ventilation. We are aware of only one prior instance of MCTD associated with unilateral diaphragmatic weakness causing mild respiratory dysfunction. To the best of our knowledge, this is the second reported case of diaphragmatic involvement in the MCTD population, with bilateral diaphragmatic paralysis causing severe respiratory failure. This is also the first reported case of such an unusual initial presentation in this patient group. Pulmonary involvement has a poor prognosis. Early diagnosis with the initiation of therapy can improve mortality outcomes in this patient population.

Bilateral diaphragmatic dysfunction: A cause of persistent dyspnea in patients with post-acute sequelae of SARS-CoV-2

Persistent shortness of breath is one of the most common concerns reported by patients with post-acute sequelae of SARS-CoV-2. Here, we present a case of bilateral diaphragmatic paralysis as a cause shortness of breath that developed after SARS-CoV-2 infection. A middle-aged gentleman with history of sleep apnea and body mass index 27.9 kg/m2 presented to our post-COVID clinic with 3 months of dyspnea and orthopnea after contracting SARS-CoV-2 in November 2020. During acute infection, he was hospitalized for hypoxemia, which improved with steroids and supplemental oxygen. At 3 months, he continued to report dyspnea and orthopnea. On examination, he had tachycardia and increased respiratory rate with paradoxical respiratory abdominal movement. Chest imaging showed elevated bilateral hemidiaphragms without any parenchymal lung disease. Pulmonary function test revealed severe ventilatory defect with restrictive lung disease. He was diagnosed with bilateral diaphragmatic dysfunction which was confirmed by absence of evoked potentials in diaphragm after phrenic nerve stimulation bilaterally. He was advised to use continuous positive airway pressure machine to assist with breathing at night. At his last follow-up (1-year post-infection), he was symptomatically improving without specific interventions.

P1‐82: Successful treatment of bilateral diaphragmatic paralysis from HIV associated axonal polyneuropathy with bilevel positive airway pressure ‐ A case report

P1‐82: Successful treatment of bilateral diaphragmatic paralysis from HIV associated axonal polyneuropathy with bilevel positive airway pressure ‐ A case report

NOT ALL THE PATIENTS PRESENTING WITH SHORTNESS OF BREATH HAVE HEART OR LUNG DISEASES

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: The diaphragm is the primary muscle of respiration. Patients with bilateral diaphragmatic paralysis can present with dyspnea on exertion and be misdiagnosed as acute heart failure. Thyroid myopathy can involve diaphragm and require a high index of suspicion in patients with symptoms of heart failure with negative workup. CASE PRESENTATION: A 47-year-old male with a past medical history of coronary artery bypass grafting, and heart failure presented with dyspnea on exertion and orthopnea for one month. He was recently admitted with the same complaints and was discharged on an increased dose of furosemide with no response. On presentation, physical exam revealed orthopnea and bilateral decreased air entry at the lung bases. Oxygen saturation was 86% on room air. Arterial blood gas results showed pH 7.31, PCO2 61 on 100% FIO2. Laboratory data, including complete blood count and comprehensive metabolic profile, were unremarkable. EKG showed normal sinus rhythm and transthoracic echocardiogram showed an ejection fraction of 62%. Chest x-ray showed elevation of right hemidiaphragm (figure-1). He was treated with intravenous Lasix and BiPAP, but symptoms didn't improve, which prompted further workup, including a fluoroscopic "sniff test," which showed the paradoxical motion of both hemidiaphragm consistent with diaphragmatic paralysis. TSH level came back 306.0 µIU/ml, free T4 level was 0.32 ng/dL. Pulmonary function tests depicted mild obstructive and moderate restrictive lung disease (figure-2). Pt was treated with levothyroxine and was discharged on levothyroxine and trilogy after symptoms started improving. He showed significant improvement at one month's follow-up. DISCUSSION: Bilateral diaphragmatic paralysis primarily presents with shortness of breath on exertion and orthopnea within minutes of recumbency. The diagnosis is challenging as symptoms can be misinterpreted as a sign of heart failure; hence it is prudent to rule out acute heart failure. Severe hypothyroidism presenting as bilateral diaphragmatic paralysis is rarely reported in the literature, which decreases the activity of acid maltase, causing thyroid myopathy. The diagnosis can be made by paradoxical motion of hemidiaphragm on "sniff test," however, the measurement of trans-diaphragmatic pressure is the gold standard. The treatment depends on etiology and severity. Hypothyroidism should be treated promptly, and the use of small portable ventilators such as trilogy are helpful to assist breathing. In patients with intact phrenic nerve with no myopathy, phrenic nerve pacing can also be considered. CONCLUSIONS: Signs and symptoms of diaphragmatic paralysis can mimic heart failure. Physicians should maintain a high index of suspicion to workup for hypothyroidism and paralysis of the diaphragm in patients with typical presentation in the absence of cardiac or pulmonary etiology, as early diagnosis and treatment have good outcomes. REFERENCE #1: Thulaseedharan NK, Geetha P, Arathi N, et al. An unusual cause of orthopnoea-hashimoto's thyroiditis presenting as bilateral diaphragmatic palsy. Respiratory Medicine Case Reports. 2017;21:132-134. doi:10.1016/j.rmcr.2017.04.016 DISCLOSURES: No relevant relationships by Shaji Baig, source=Web Response No relevant relationships by Aneeba FAROOQi, source=Web Response No relevant relationships by Hafiz Jeelani, source=Web Response

Diaphragm dysfunction (paralysis) in a cystic fibrosis patient

Diaphragmatic paralysis (DP) is a rare disease and usually occurs secondary to systemic processes, although idiopathic forms have been described. Management of diaphragmatic paralysis depends on multiple factors, including the etiology, presence, or absence of symptoms, and more importantly, the presence of nocturnal hypoventilation. DP has been described in both unilateral and bilateral forms. In unilateral DP, most patients are asymptomatic and often do not require intervention. Symptomatic patients with unilateral DP, however, will require plication. In bilateral DP, phrenic nerve pacing or nasal continuous positive airway pressure, bilateral positive airway pressure (CPAP BiPAP), or intermittent positive pressure ventilation by the nasal or oral mask is recommended. We describe a case of unilateral DP in a cystic fibrosis patient treated by surgical plication.

Diaphragm Dysfunction (Paralysis) in a Cystic Fibrosis Patient

Diaphragmatic Paralysis (DP) is a rare disease and usually occurs secondary to systemic processes, although idiopathic forms have been described. Management of diaphragmatic paralysis depends on multiple factors, including the etiology, presence, or absence of symptoms, and more importantly, the presence of nocturnal hypoventilation. DP has been described in both unilateral and bilateral forms. In unilateral DP, most patients are asymptomatic and often do not require intervention. Symptomatic patients with unilateral DP, however, will require plication. In bilateral DP, phrenic nerve pacing or nasal Continuous Positive Airway Pressure, Bilateral Positive Airway Pressure (CPAP BiPAP), or intermittent positive pressure ventilation by the nasal or oral mask is recommended. We describe a case of unilateral DP in a cystic fibrosis patient treated by surgical plication.

Delayed presentation of bilateral diaphragmatic palsy following trauma

Delayed presentation of bilateral diaphragmatic palsy following trauma

Instant orthopnea and pseudo-cardiac dilatation due to anterior mediastinal tumor.

A 45-year-old woman presented with instant orthopnea and enlarged cardiomediastinal silhouette in her chest radiograph. Although anterior mediastinal tumor can be misdiagnosed as heart failure due to orthopnea with enlarged cardiomediastinal silhouette, "instant orthopnea" may be a useful sign to distinguish these conditions.

Pectoralis Minor Activity in a Rodent Model of Respiratory Motor Neuron Loss

Patients with neuromuscular diseases experience loss of respiratory motor neurons (i.e., phrenic and intercostal) resulting in ventilatory failure, and ultimately death. No treatment is currently available to significantly prolong and/or improve breathing in these diseases. Since genetic rodent models of motor neuron loss develop global symptoms (e.g., dysphagia, limb paralysis, etc.), we have developed an inducible model of only respiratory motor neuron death in order to study how motor neuron loss impacts respiration and to develop therapeutic interventions. Briefly, adult rats are intrapleurally injected with cholera toxin B conjugated to saporin (CTB‐SAP) that is retrogradely transported to the phrenic and intercostal motor nuclei of the spinal cord, which results in selective elimination of phrenic and intercostal motor neurons. Despite deficits in maximal ventilatory capacity following CTB‐SAP, eupneic ventilation is maintained. Our preliminary data suggest that one way eupnea may be maintained in CTB‐SAP rats is via the recruitment of G‐coupled protein receptor‐dependent pathways to cause respiratory plasticity in the phrenic motor nucleus over the course of phrenic motor neuron death. However, our preliminary data also indicate that diaphragmatic amplitude appears to be decreased at baseline in CTB‐SAP rats vs. controls; thus, phrenic respiratory plasticity may only account for a portion of the maintenance of eupneic ventilation. We speculate that eupnea is also maintained through the recruitment of accessory inspiratory muscles (e.g., the pectoralis minor muscles) in the face of respiratory motor neuron loss. Pectoralis minor muscles are not normally utilized for eupnea, but have been shown to increase their activity to actively elevate the ribs upward and outward to move the chest wall following increased ventilatory demand (e.g., in response to disease or injury including spinal cord injury and bilateral diaphragmatic paralysis). Thus, we hypothesize that pectoralis minor activity is increased over the course of respiratory motor loss in CTB‐SAP rats vs. controls. To test our hypothesis, we are studying pectoralis minor output via electromyography in anesthetized, spontaneously breathing control and CTB‐SAP adult rats. Our preliminary data indicate that pectoralis minor activity appears to be increased in CTB‐SAP rats vs. controls (n=4/group). Thus, we conclude that the pectoralis minor muscles may also be recruited to maintain eupneic ventilation in the face of respiratory motor neuron death. Future studies will evaluate the recruitment of other accessory inspiratory muscles (e.g., scalenes, sternocleidomastoid, etc.) over the course of respiratory motor neuron loss, and whether these muscles (including the pectoralis minor) are necessary for eupnea in CTB‐SAP rats. This study furthers our understanding of the potential contribution accessory inspiratory muscles, specifically the pectoralis minor, have on the maintenance of eupneic ventilation following respiratory motor neuron loss. Lastly, if our hypothesis is correct, these muscles could potentially be further stimulated and harnessed to significantly prolong and/or improve breathing in patients with neuromuscular disease.Support or Funding InformationMissouri Spinal Cord Injury/Disease Research Program

Bilateral Isolated Phrenic Neuropathy: a Rare Cause of Dyspnoea

Bilateral diaphragm paralysis due to bilateral isolated phrenic neuropathy (BIPN) is a very rare cause of unexplained respiratory failure.We present a 65-year-old patient with no relevant previous medical history who presented in the Pulmonology Clinic with mMRC1 dyspnoea and orthopnoea. After the medical work-up, diaphragmatic paresis was diagnosed. Inspiratory muscle training resulted in mild symptomatic improvement and treatment with noninvasive mechanical ventilation (NIV) was initiated.This condition is generally chronic and has a poorer prognosis, compared to other cases of phrenic nerve involvement. In this case, NIV restored near-normal daily function.LEARNING POINTSBesides being a rare cause of dyspnoea, diaphragmatic dysfunction should be considered in the medical evaluation.Noninvasive mechanical ventilation is the mainstay of treatment for symptomatic patients.Neurologic and electrodiagnostic evaluation is essential, since the differential diagnosis of phrenic nerve dysfunction may imply different treatment strategies.

Phrenic nerve palsy: A rare cause of respiratory distress in newborn: A literature review

Phrenic nerve palsy could result from multiple etiologies including birth injuries. It could often be associated with brachial plexus palsy. The phrenic nerve plays a major role in innervating the diaphragm. It is the only motor supply to the diaphragm and also acts a sensory nerve. In this palsy, the patient may present with diaphragmatic dysfunction, unilateral diaphragmatic paralysis, or bilateral diaphragmatic paralysis. This diaphragmatic paralysis caused by phrenic nerve injury could lead to respiratory distress in the newborn. Thus, a newborn with respiratory distress and an elevated hemidiaphragm should be suspected for phrenic nerve palsy in the imaging studies and also in the differential diagnosis of respiratory distress in a newborn presenting with a history of traumatic delivery or brachial plexus palsy. We also herein report a case of phrenic nerve palsy in a newborn presenting with respiratory distress.

Une paralysie diaphragmatique bilatérale révélant une neuroborréliose de Lyme

Lyme disease is not uncommon and can sometimes progress to neurological complications. We report here an unusual case of bilateral diaphragmatic paralysis secondary to Lyme neuroborreliosis. A 79-year-old man was admitted to the intensive care unit for acute respiratory distress requiring intubation and the long-term use of nocturnal non-invasive ventilation. Three months beforehand he had been bitten by a tick and developed erythema migrans which was treated with Doxycycline for 10days. This clinical presentation became complicated a few days later by the progressive onset of severe dyspnoea. At admission, chest radiography revealed bilateral elevation of the diaphragm. Pulmonary function tests revealed a severe restrictive disorder aggravated by decubitus. A diaphragmatic electromyogram showed bilateral axonal polyneuropathy of the phrenic nerves. IgG and IgM antibodies to Borrelia burgdorferi were detectable in serum and cerebrospinal fluid, leading to the diagnosis of Lyme disease. He was treated with intravenous ceftriaxone 2g per day for 21days, leading to a substantial improvement in symptoms. In the presence of unilateral or bilateral diaphragmatic paralysis of undetermined aetiology, it seems relevant to perform Lyme serology in the blood and, in positive cases, to follow up with a lumbar puncture in order to detect intrathecal IgG synthesis.

Bilateral diaphragmatic palsy in a parturient for emergency Caesarean delivery - What are our concerns?

Bilateral diaphragmatic palsy in a parturient for emergency Caesarean delivery - What are our concerns?