Can patent foramen ovale affect rehabilitation? The uncommon association of platypnea-orthodeoxia syndrome and stroke.

Platypnea-orthodeoxia is a rare syndrome characterized by dyspnea and deoxygenation induced by a change to a sitting or standing from a recumbent position. It is the result of posturally accentuated intracardiac or pulmonary right-to-left shunt leading to arterial oxygen desaturation. Only few cases of platypnea-orthodeoxia syndrome are reported in the literature and the association between stroke and platypnea-orthodeoxia syndrome with evidence of patent foramen ovale is extremely rare. We describe the case of a 67-year-old female admitted to our Rehabilitation Unit for disabling basilar stroke due to paradoxical embolism from patent foramen ovale that during the first days of rehabilitation showed signs and symptoms of platypnea-orthodeoxia syndrome. To remove a life-threatening condition for the patient and in order to develop the normal rehabilitation project, that was stopped by the platypnea-orthodeoxia syndrome, the patient fastly underwent to percutaneous closure of patent foramen ovale. The stabilization of oxygen arterial saturation with postural changes and the disappearance of symptoms of POS allowed to develop the rehabilitation project with progressive neurological improvement.

Contralateral diaphragmatic palsy after subcortical middle cerebral artery infarction without capsular involvement.

Diaphragmatic palsy after acute stroke is a novel clinical entity and may result in a high incidence of respiratory dysfunction and pneumonia, which especially cause greater morbidity and mortality. Generally, internal capsule and complete middle cerebral artery (MCA) infarctions are major risk-factors for developing diaphragmatic palsy. Herein, we present a case with contralateral diaphragmatic palsy after a subcortical MCA infarction without capsular involvement. Dyspnea occurred after stroke, while a chest X-ray and CT study disclosed an elevated right hemidiaphragm without significant infiltration or patch of pneumonia. A phrenic nerve conduction study showed bilateral mild prolonged onset-latency without any significant right-left difference. This suggested a lesion causing diaphragmatic palsy was not in the phrenic nerve itself, but could possibly originate from an above central location (subcortical MCA infarction). We also discussed the role of transcranial magnetic stimulation study in the survey of central pathway and demonstrated diaphragmatic palsy-related orthopnea.

Dyspnoeic dysphasia: a series of unfortunate events.

We describe a case of a 56 year old man with no previous medical history who presented with sudden onset dyspnoea, expressive dysphasia, and right arm sensory loss and paresis. A diagnosis of bilateral pulmonary embolism and transient cerebral ischaemic attack was confirmed by CT pulmonary angiogram and MRI. Paradoxical embolism through an occult patent foramen ovale (PFO) was subsequently proven by contrast echocardiography. This case highlights a number of short and long-term management conundrums, that to date are incompletely addressed by clinical trials. These include timing of anticoagulation in patients with both venous thromboembolism and cerebral infarction, and the risk:benefit ratio of surgical closure of patent foramen ovale.

Paroxysmal dyspnea in Parkinson's disease: Respiratory dyskinesias and autonomic hyperventilation are not the same.

Respiratory complaints are not uncommon in patients with Parkinson's disease (PD). While many are explained by pulmonary and cardiovascular problems unrelated to PD, secondary effects of PD, such as kyphoscoliosis, respiratory muscle rigidity, repeated pneumonias, or side effects of medication such as dyskinesias, there is a small group of patients with paroxysmal dyspnea for whom neither anxiety or other explanation has been found. This Point of View was written to call attention to this neglected, uncommon, but very distressing symptom.

Alveolar membrane conductance decreases as BNP increases during exercise in heart failure. Rationale for BNP in the evaluation of dyspnea.

BACKGROUND: In left ventricular failure (LVF) patients, brain natriuretic peptide (BNP), lung diffusion for carbon monoxide (DLCO), and alveolar-membrane conductance (DM) correlate with LVF severity and prognosis. The reduction of DLCO and DM during exercise reflects pulmonary edema formation. METHODS AND RESULTS: To evaluate, in LVF patients, the correlation between BNP and lung diffusion parameters at rest and during exercise, we studied 17 severe LVF patients, 13 moderate, and 10 normals measuring BNP and lung diffusion parameters before, at the end, and 1 hour after a 10-minute high-intensity constant-workload exercise. At rest, a significant correlation exists between BNP and lung diffusion parameters. Resting BNP, DLCO, and DM correlate with peak oxygen consumption (P < .0001 for all analyses). With exercise, BNP increase is significant (severe LVF 180 +/- 49 pg/mL, moderate 68 +/- 58, normals 18 +/- 12); differently, only in severe LVF, with exercise, DLCO (-1.1 +/- 0.7 mL/mm Hg/min, P < .0001) and DM (-6.4 +/- 2.8, P < .0006) decrease. One hour after exercise, only in severe LVF, BNP is still higher than at rest, while DLCO, DM, and DM/Vc are lower. Significant correlations are observed between BNP and DM changes during exercise and recovery (P < .0001) in severe LVF. CONCLUSIONS: In severe LVF, BNP changes during exercise correlate with simultaneous reductions in DM, suggesting that BNP increase and pulmonary edema formation could be related.

Emergency department evaluation and management of peripartum cardiomyopathy.

Peripartum cardiomyopathy (PPCM) affects 1000-1300 women in the United States each year. We present three cases of PPCM seen in our Emergency Department (ED) that cover the entire spectrum of disease from mild heart failure to sudden cardiac death. Without previous heart disease, these women develop cardiomyopathy with impairment of left ventricular function in the last month of pregnancy, or during the first 5 months postpartum. The etiology of PPCM is not clear, although various mechanisms have been proposed, including infection, autoimmune response, prolonged tocolysis during labor, and maladaptive responses to the hemodynamic changes of pregnancy. The initial presentation of these patients is frequently to the ED. The differential diagnosis and key characteristics of PPCM are discussed. ED management should focus on three elements: reduction in pre-load, reduction in afterload, and increase in inotropy. Key differences between the antepartum and postpartum states are highlighted.

[Gastroesophageal reflux: a possible cause of paroxysmal laryngeal dyspnea]. / La dyspnée laryngée paroxystique: une manifestation extra-oesophagienne peu connue du reflux gastro-oesophagien.

An important number of patients are referred to the ENT specialist because of extraoesophageal manifestations of gastroesophageal reflux. The most alarming symptom is a paroxysmal dyspnea secondary to a laryngospasm. The patients report a laryngeal choking sensation associated to an aphonia. We report three cases of laryngospasm secondary to acid gastric reflux. The diagnosis was made with the clinical history, a laryngeal examination and a 24-hour pH-monitoring enabled us to demonstrate a clear temporal relation between the reflux episodes and the choking episodes. In conclusion, the pharyngo-laryngeal reflux is a possible cause of laryngospasm. In our three patients, a high dose antiacid treatment was efficient to bring a lasting relief of the symptoms.

A 58-Year-Old Man With Position-Dependent Nocturnal Dyspnea.

CASE PRESENTATION: A 58-year-old man with idiopathic pulmonary fibrosis, who had received a right-sided single-lung transplant 2 years earlier, was referred to the sleep clinic for the assessment of nocturnal position-dependent episodes of dyspnea and frequent arousals when lying on his right side. There was no subjective worsening of daytime respiratory symptoms, but he complained of fatigue and unrefreshing sleep. His Epworth Sleepiness Scale score was 12/24. After lung transplantation he had a favorable course while receiving immunosuppression with prednisolone, everolimus, and mycophenolate mofetil. In addition, he had received diagnoses of stable coronary artery disease and moderate chronic kidney failure.

Oropharyngeal chordoma diagnosed by fine needle aspiration: a case report.

BACKGROUND: Due to its rarity, chordoma may be difficult to differentiate from other neoplasms with a similiar myxoid background. We describe a case of chordoma involving the oropharynx inferiorly that was diagnosed by transoral fine needle aspiration (FNA) cytology (FNAC) and confirmed by histologic studies. This appears to be 1 of the few reported applications of FNA in the diagnosis of chordoma of the oropharynx in the English-language literature. CASE: A 50-year-old male presented with nocturnal dyspnea and rare hemoptysis for 6 months. A hypodense mass was located in the left posterior side of the oropharynx. FNAC of the mass showed classic physaliferous cells with a bubbly appearance and myxoid fibrillary background. The aspirate was reported as "myxoid tumor suggestive of chordoma," as confirmed by histopathologic investigation of the excisional biopsy. CONCLUSION: The cytologic features of chordoma are quite characteristic, especially on May-Grünwald-Giemsa (MGG)-stained slides. The cytoplasmic vacuoles of the physaliferous cells and the mucoid matrix of the tumor become conspicuous on MGG staining. When Papanicolaou staining is used as the only staining procedure, the cytoplasmic vacuoles of the physaliferous cells and mucoid matrix of chordomas may be overlooked. The differential diagnosis of myxoid tumors is of utmost importance for therapy and prognosis.

Massive right atrial myxoma with dyspnea at rest in an elderly patient: a case report.

INTRODUCTION: Primary heart tumors are extremely rare and myxoma is the most common type of these tumors. Although intra-atrial presentation is a predilection place, right atrial localization is atypical. The symptom triad is characteristic in the clinical presentation of the tumor: embolic complication, intracardiac blood flow obstruction and systemic manifestations like elevated erythrocyte sedimentation rate, fever, anemia, body weight loss. CASE REPORT: We presented an elderly female patient with massive myxoma in the right atrium, 77 x 44 mm in diameter, which filled the entire right atrium and spread into the right ventricle, causing the tricuspid valve obstruction and dyspnea. It was visualized by transthoracic echocardiography and small and insignificant pericardial effusion was also seen. After surgical removal of the tumor, the patient remained without any symptoms and pericardial effusion. CONCLUSION: Tumors of the right heart have to be considered in the differential diagnosis of unexplained dyspnea in elderly patients. Transthoracic echocardiography is certainly necessary and mostly available diagnostic tool that can be of great help in diagnosing heart tumor as well as planning cardiac surgery, as it provides in most cases excellent visualization of the tumor and its relationship with other parts of the heart.

Bronchial hyperresponsiveness to inhaled methacholine in subjects with chronic left heart failure at a time of exacerbation and after increasing diuretic therapy.

Cough and wheezing are common findings in left heart failure. However, it is still questionable whether nonallergic bronchial hyperresponsiveness, the hallmark of asthma, is also associated with this condition. In 12 subjects with acute decompensation of chronic postischemic LV failure, we assessed the PC20 methacholine during an episode of acute LV failure and after five to 15 days of intensive diuretic therapy. Weight, arterial blood gases, plethysmographic lung volumes, and expiratory flows were also measured on both visits. Extravascular lung water was estimated indirectly with a radiologic score. During acute decompensation, six subjects had significant airway obstruction and eight had a PC20 less than or equal to 16 mg/ml (significant bronchial hyperresponsiveness). After diuretic therapy, subjects improved significantly, losing an average of 2.2 kg, but they still had chronic LV failure and evidence of an obstructive breathing defect. Although mean PC20 was unchanged, three subjects had significantly improved PC20 after treatment. We conclude that: (1) left ventricular failure is often associated with mild bronchial hyperresponsiveness, although it is not excluded that smoking and the resulting possibility of bronchial obstruction can also play some role; and (2) acute treatment does not generally alter bronchial responsiveness to methacholine, suggesting that chronic LV failure can cause chronic changes to the airways.

Effect of posture on bronchial reactivity to inhaled methacholine in patients with mitral valve stenosis.

To compare the effects of posture on bronchial reactivity in 12 patients with mitral valve stenosis (MS) and 10 with bronchial asthma (BA), a methacholine inhalation test was performed 2 h after being in either a supine or sitting position. All patients showed bronchial hyperreactivity to inhaled methacholine before the study. In MS patients, logarithmic values of the cumulative dose producing a 35 percent decrease in respiratory conductance (log PD35Grs) were significantly lower 2 h after being in a supine position than in those after being in a sitting position (0.71 +/- 0.78, 1.02 +/- 0.53 log units, respectively, p < 0.05). In BA patients, however, log PD35Grs did not show significant changes (0.42 +/- 0.51, 0.58 +/- 0.48 log units, respectively). Variables of pulmonary function tests showed no significant differences between the two positions in both patients with MS and BA. We conclude that the bronchial hyperreactivity in MS is enhanced after the supine position for 2 h and that the supine posture may play an important role in the pathogenesis of cardiac asthma.

Pedicled pericardial patch repair of a carinal bronchogenic cyst.

Bronchogenic cysts should be completely removed. Small communications with the tracheobronchial tree occur, but extensive involvement is rare. A case of bronchogenic cyst replacing the carina and the medial wall of the right and left main bronchi is presented. Resection and reconstruction was accomplished by using a pedicled pericardial patch to close the defect created by removal of the bronchogenic cyst. Follow-up at 2 years shows an excellent result.

Dyspnea in the elderly: cardiac or pulmonary?

Compare the chest film with previous films, if possible. Changes in heart size and interstitial and vascular markings can thus be seen more readily, as can air trapping; this also aids in differentiation of acute from chronic changes. A Holter monitor study should be obtained if dyspnea occurs irregularly, has acute onset and termination, or is associated with dizziness or syncope; or if the resting ECG shows frequent premature atrial contractions, premature ventricular contractions, bradycardia, or periods of advanced heart block.

Nebulized morphine for paroxysmal cough and dyspnea in a nursing home resident with metastatic cancer.

Nursing homes continue to be challenged with the task of caring for patients in various stages of disease. Historically, the death of a long-term care patient in this setting is not unusual; however, researchers and clinicians are focusing increasingly on the quality of life at the end of life, regardless of location. The long-term care facility is an ideal setting in which to begin to effectively address these issues, especially as individual patients in need present for care. Although the care of many of our geriatric patients meets the definition of palliative care, no where is the need greater, and more obvious, than in the patient presenting with terminal illness. Aggressive treatment of distressing symptomatology contributes to overall quality of life, and returns to the patient some of the freedom and autonomy usurped by the disease process. It is particularly rewarding for the interdisciplinary team to be successful in controlling symptoms in the patient with limited life expectancy, thus allowing the patient to complete unfinished tasks and enjoy quality time with family and friends. Often the "triumphs" in the nursing home are few and fleeting; abolishing pain, distress, and suffering is both personally and professionally satisfying for everyone involved. We presented a review of the available literature on a technique in palliative medicine which is still evolving. Additional, we presented its practical use in a frail, elderly nursing home resident admitted with end-stage metastatic breast carcinoma. The geriatric adage of "start low, and go slow" was effectively borne out in the management of this resident's most difficult symptoms, shortness of breath and paroxysmal cough leading to symptomatic atrial fibrillation. The key to the management of the frail elderly patient goes beyond " start low and go slow" to "aggressively titrate as needed but no further" in order to meet the needs of the individual patient and avoids unwanted side effects.

[Paroxysmal nocturnal dyspnea as a severe expression of the pacemaker syndrome]. / Dispnea notturna paradossa come severa espressione di sindrome da pacemaker.

Single-chamber ventricular pacing remains a frequent pacing method for symptomatic bradyarrhythmias. VVI pacing is effective in maintaining an acceptable ventricular rate, preventing severe bradycardia. However it may cause many important symptoms as a consequence of loss atrio-ventricular synchrony. Pacemaker syndrome (i.e. symptoms and signs caused by inadequate timing of atrial and ventricular contractions) may range in severity from vague pacing awareness to congestive heart failure. This event may be related more to retrograde ventricular-atrial conduction than to the absence of atrio-ventricular synchrony. We report 2 cases of VVI pacing complicated by nocturnal dyspnea (sign of congestive heart failure) as severe manifestation of pacemaker syndrome. By implantation of dual-chamber pacemaker, atrio-ventricular synchrony was restored, nocturnal dyspnea disappeared and has not recurred during clinical follow-up (12 and 4 months respectively for the first and second case.