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Query: UMLS:C0476273 (respiratory distress)
 19,632 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The term adult respiratory distress syndrome (ARDS) was first introduced by Ashbaugh and Petty more than two decades ago. Since then, our understanding of this clinicopathologic entity has increased significantly. However, little therapeutic progress has been achieved, and the mortality remains high. ARDS is characterized by diffuse pulmonary microvascular injury resulting in increased permeability and, thus, noncardiogenic pulmonary edema. Ventilation-perfusion lung studies have demonstrated that the predominant pathogenesis of hypoxemia in ARDS is related to intrapulmonary shunts. Common symptoms include dyspnea, tachypnea, dry cough, retrosternal discomfort, and moderate to severe respiratory distress. In most cases the diagnosis of ARDS is that of exclusion. The mainstay of therapy for this syndrome is the management of the underlying disorder causing it. To date, there are no specific pharmacologic interventions of proven value for the treatment of ARDS. Once the potentially treatable sources have been found and their therapy started, the main treatment for ARDS is supportive.
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PMID:Adult respiratory distress syndrome (ARDS): the basics. 816 9

We reported two cases of idiopathic interstitial pneumonia (IIP) who developed acute exacerbation after bronchoalveolar lavage (BAL). One case was a 67-year-old male who presented with dry cough and exertional dyspnea. He was diagnosed as IIP and transbronchial lung biopsy revealed alveolitis. BAL was performed after administration of prednisolone. He complained of severe dyspnea after BAL and was diagnosed as having an acute exacerbation of IIP. In spite of extensive treatment including pulse therapy with methylprednisolone, he died. The other case was a 57-year-old male noted to have a chest X-ray abnormality who presented with dry cough and dyspnea on exertion. He was diagnosed as having IIP and primary lung cancer. BAL was performed to evaluate the activity of IIP, and respiratory distress subsequently became severe. After BAL, he developed an acute exacerbation of IIP and died in spite of treatment. In both cases, peripheral white blood cell counts were increased just before BAL. It was suggested that this condition might participate in acute exacerbation of IIP. It should be kept in mind that some patients with IIP may develop acute exacerbation after BAL.
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PMID:[Two cases of IIP which developed acute exacerbation after bronchoalveolar lavage]. 816 6

In this report, we present 2 cases of severe congestive heart failure and mild renal insufficiency in patients who underwent continuous ambulatory peritoneal dialysis (CAPD) after stabilization using the extracorporeal ultrafiltration method (ECUM). Long-term good control of congestive heart failure was achieved following the institution of CAPD. Case 1, a 58-year-old woman with rheumatic arthritis and diabetes mellitus had anteroseptal myocardial infarction at the age of 52. And case 2, a 68-year-old man, who underwent coronary artery bypass surgery at the age of 66 and had extensive anterior infarction after the operation. They were admitted to the hospital with dyspnea due to congestive heart failure. In both cases, systolic cardiac function was severely impaired and mild renal insufficiency was present at the time of hospitalization. After admission, symptomatic relief was not obtained by conventional therapies and symptoms of congestive heart failure worsened until the patients suffered from severe respiratory distress even at rest. ECUM was then instituted to remove excess fluid and clinical improvement was achieved. After the initiation of ECUM, responsiveness to diuretics was not restored, and the procedure was necessary every day or every other day for the prevention of symptoms due to fluid overload. About 20 days after the initiation of ECUM, CAPD was begun for the long-term control of congestive heart failure and renal failure, and for the purpose of hospital discharge. Good control of heart failure was achieved after the initiation of CAPD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Two case reports of refractory heart failure treated by continuous ambulatory peritoneal dialysis]. 823 16

Pulmonary edema (PE) which is similar to the neurogenic type was induced by adrenaline (AD) administration (0.1 mg/kg) in rats. Acute progressive respiratory distress, cyanosis and dyspnea occurred. All the experimental animals in the PE group died within 20 min after AD injection, with a pulmonary index (PI) of 1.70 +/- 0.47 (mean +/- S) which was much higher than that in the normal group. The mortality rate was 100%. It was found that in rats with PE, a protein-rich fluid filled the alveolar and interstitial spaces, and ecchymosis occurred. The capillary permeability as estimated by Evans blue injection showed that Evans blue from extraction fluid and bronchoalveolar lavage (BAL) in the PE rats was at a much higher level than that in the normal control (NC) rats. In anisodamine (ADM, 654-2) and tetramethylpyrazine (TMP) treated rats, almost all the damage was diminished or absent, and the mortality rates were decreased from 100% to 4.4% and 20%, respectively. 654-2 and TMP could significantly inhibit the increase of pulmonary permeability.
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PMID:Hemodynamic and nonhemodynamic mechanisms of experimental pulmonary edema in rats and the effect of anisodamine and tetramethylpyrazine. Part 1: Survival rate, pulmonary index, pathological change and pulmonary vascular permeability. 829 2

A case of hereditary motor and sensory neuropathy (HMSN) type 1 (Charcot-Marie-Tooth disease (CMT)) is reported with vocal cords palsy, deafness, diaphragmatic weakness, and cerebellopontine atrophy. A 42-year-old man was admitted to our hospital in April, 1991 with marked respiratory distress. He had been diagnosed as having CMT 14 years previously. On admission to our hospital, he revealed dyspnea with marked stridor during inspiration. Physical examination showed marked use of respiratory accessory muscles with thoracoabdominal paradox in the supine position. Neurologic examination revealed tonic pupils, mild bilateral weakness of facial muscles, deafness, mild bulbar palsy, severe wasting and weakness in both proximal and distal muscles of the arms and legs, areflexia, distal loss of all sensory modalities. Pes cavus and hammer toe were present. Movement of upper extremities was ataxic. No hypertrophic changes were noted in his peripheral nerves. Peripheral nerve conduction study showed undetectable both sensory and motor action potentials. Electromyography showed evidence of denervation, more marked in distal muscles. Auditory brain stem response was undetectable. Chest radiographic film showed a normal-sized heart with marked elevation of both hemidiaphragm. Laryngofiberscopy confirmed the presence of bilateral vocal cord paralysis without tumor formation, inflammation or anomaly. The vocal cords lay near the midline and did not show any movement during respiration. Moderate cerebellopontine atrophy was confirmed on MRI scan. A sural nerve section showed severe decrease of myelinated fibers, and onion bulbs. Diagnosis of HMSN type 1 was made by clinical, electrodiagnostic, and sural nerve sections study.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of hereditary motor and sensory neuropathy with vocal cords palsy and diaphragmatic weakness]. 831 89

A prospective study of 222 consecutive autopsies of cancer cases was undertaken to investigate whether carcinomatous lymphangitis and pure arterial tumor embolism of the lungs are different clinicopathological entities. The lungs were removed as a block and 15 sections (three from each lobe) were analyzed. A protocol containing clinical (ie, dyspnea, cyanosis, right ventricular failure, engorgement of jugular veins, and peripheral edema as main cause of death) and morphological (ie, right ventricle thickness and dilatation, vascular sclerosis, pulmonary infarct) data were carefully recorded in each case. Arterial tumor embolism was detected in 19 cases (8.5%) and carcinomatous lymphangitis in 44 cases (19.8%). We found no differences in relation to signs and symptoms of arterial tumor embolism and carcinomatous lymphangitis, but respiratory distress as the main cause of death was significantly more frequent in the cases with arterial involvement by tumor emboli. Morphologically, however, right ventricular hypertrophy-dilatation, histological signs of pulmonary hypertension, and hemorrhagic infarcts were more prevalent in the cases with arterial tumor embolism. This study permits us to conclude that although arterial tumor embolism and carcinomatous lymphangitis are clinically similar diseases, they are morphologically different entities. Our results suggest that the most probable pathogenesis of pulmonary endarteritis and subsequent pulmonary hypertension is the injury to the vascular endothelium caused by the arrest of tumor emboli.
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PMID:Pulmonary tumor embolism to arterial vessels and carcinomatous lymphangitis. A comparative clinicopathological study. 834 48

A 22-year-old female patient with an 8-year history of mixed connective tissue disease (systemic sclerosis overlapping with systemic lupus erythematosus) presented with marked respiratory distress, sinus tachycardia (135 bpm), and pulsus paradoxus. The chest x-ray showed an enlargement of the cardiac silhouette, which was due to a 3-cm-wide, circular pericardial effusion, as demonstrated by two-dimensional echocardiography. Pericardiocentesis performed to decompress cardiac tamponade did not lead to clinical improvement. The increase in dyspnea was caused by a rise in pulmonary wedge pressure from 21 to 40 mm Hg following an acute increase of mitral valve regurgitation. In the presence of global hypokinesia of the left ventricle, cardiac output decreased from 3.25 to 2.63 l/min. Intensive care including hemodialysis and plasmapheresis as well as high-dose application of cyclophosphamide and steroids led to a stabilization of the hemodynamic situation over a period of days. The case report presented here supports the general recommendation to perform pericardiocentesis in a stepwise manner under hemodynamic monitoring. This holds true primarily for patients with mitral valve regurgitation and/or cardiac involvement in connection with an underlying disease.
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PMID:[Pulmonary edema as a complication during pericardial puncture in "mixed connective tissue disease"]. 835 45

Airway disruptions after blunt chest trauma are rather infrequent with an incidence of about 1%. Even in large centers with many such casualties they are episodical. The clinical picture is not an uniform one, and typical clinical signs occur often without an airway lesion. Therefore, the correct diagnosis may be delayed. Two case reports, one with a tracheal rupture, the other with complete disruption of the main right bronchus are presented. Both patients showed significant soft tissue emphysema, increasing dyspnea and hypoxia respectively within a few hours after their accident. The diagnosis was established bronchoscopically after time intervals of 8 and 32 hours respectively, followed by immediate surgical correction. Both patients experienced a smooth recovery with good longterm results. In blunt chest trauma presenting with subcutaneous emphysema, pneumomediastinum, pneumothorax, hemoptysis and respiratory distress, tracheobronchial disruption should be considered. In this case, expert bronchoscopy, preferably by a surgeon with large thoracic experience, is mandatory.
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PMID:[Tracheal and bronchial rupture after blunt thoracic trauma]. 845 88

We used Expandable Metallic Stent (EMS) to bilateral bronchial stenosis due to invasion of lung cancer. A 75-year-old man was admitted to our hospital because of dyspnea and a fainting fit on October 19, 1991. He had been suffered from squamous cell carcinoma of right lung with bilateral bronchial invasion (T4N2M0), which has no indication for surgery. As the stenosis of bilateral main bronchus and the respiratory distress progressed, we applied EMS to the patient and inserted it into the left main bronchus on December 19, 1991. The procedure promptly relieved the respiratory distress and improved his quality of life. Bronchial endoscopy, performed on the 20th postoperative day, revealed the left bronchus patency. Thus, EMS applied to the bronchial stenosis caused by advanced lung cancer may be a choice of palliative therapy and can improve the quality of patient's life.
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PMID:[Usefulness of expandable metallic stent to bronchial stenosis caused by an advanced lung cancer--a case report]. 851 75

From 1977 to 1992, 23 patients with primary tumors of the trachea were reviewed. Nineteen of these patients had squamous cell carcinomas, 2 had adenoid cystic carcinomas, 1 had a small cell carcinoma, 1 had a poorly differentiated carcinoma, and 1 had a pleomorphic adenoma. The prognosis of squamous cell, small cell and poorly differentiated carcinomas appeared to be grave, especially in association with vocal cord palsy (26%). Short-term survival occurred in 7 to 9 patients with tumors in the upper-middle third of trachea and 4 of them had concurrent acute respiratory distress. Cough (65.2%), dyspnea (91.3%), and hemoptysis (47.8%) were the most common symptoms. For patients with hoarseness, dysphagia, and cervical lymphadenopathy, the prognosis was poor (p < 0.0010). Two patients (8.7%) had multiple malignancies and all died within 1 year. Smoking was not only a risk factor as reported in previous studies, but also a significant prognostic factor (p = 0.0020) in our series. Emergent irradiation ( < 40 Gy in our cases) was useful in alleviating acute respiratory distress, but worthwhile survival was only obtained by the combination of surgery and radiation therapy (p = 0.0200, compared with surgery or irradiation, respectively). There was a significant correlation between prognosis and histologic type, tumor location, clinical presentation, smoking history and management, but not roentography or tumor size. These factors can be used to assess the survival of patients with primary tracheal tumors.
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PMID:Descriptive study of prognostic factors influencing survival of patients with primary tracheal tumors. 852 32


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