Long-term continuous infusion of labetalol.
Explore the source record for details and available documents.
Adult↗
Biomedical subjects
S A Sahn
Publications and source records attributed to S A Sahn.
Metastatic choriocarcinoma of the lung presenting as hemothorax.
Explore the source record for details and available documents.
Adult↗
Miliary tuberculosis presenting as hepatic and renal failure.
A 67-year-old man developed hepatic and renal failure over a six-day period. Despite full supportive measures, he died on his 11th day of hospitalization with fulminant DIC and hepatic, renal, and respiratory failure. Postmortem examination revealed acid-fast bacilli in virtually all organ systems. Miliary tuberculosis should be considered as a potentially treatable cause of hepatic failure.
Acute Kidney Injury↗
Benign thyroid hyperplasia presenting as bilateral vocal cord paralysis. Complete remission following surgery.
A 52-year-old woman developed respiratory arrest on two separate occasions that required mechanical ventilation. Fiberoptic bronchoscopy demonstrated bilateral vocal cord paralysis, and a CT scan of the neck demonstrated a right neck mass. On surgical exploration, the mass was found extending from the thyroid gland and was identified as benign thyroid tissue. Thyroid hyperplasia should be considered in the differential diagnosis of bilateral vocal cord paralysis.
Female↗
Continuous lateral rotational therapy and nosocomial pneumonia.
The adverse effects of prolonged immobility are due primarily to gravitational effects on blood flow and ventilation, impairment of the normal mucociliary escalator and possibly an increase in extravascular lung water. However, CLRT theoretically should reverse these abnormalities. The sequence of events that culminate in LRTI or pneumonia is unclear; however, low tidal volumes, increased extravascular lung water and the accumulation of bronchopulmonary secretions may lead to atelectasis, a well-known precursor of pneumonia. Three prospective, randomized studies evaluating patients with acute head trauma, orthopedic injuries requiring traction and blunt chest trauma all showed a decreased incidence of LRTI or pneumonia with CLRT compared with those treated in a conventional bed and turned every 2 h by the nursing staff. In general, the methodology was sound with early randomization, use of precise criteria to define LRTI and pneumonia and appropriate observation. The fourth study performed in a medical ICU with a heterogeneous group of patients did not show a difference in incidence of nosocomial pneumonia between treatment in CLRT and a conventional bed, but did show a decreased length of ICU stay for patients with pneumonia treated with CLRT. It appears that if CLRT is to be effective, it needs to be instituted early in the patient's illness. The length of time that CLRT should be utilized is unknown; however, intuitively, as long as the patient is at risk, the therapy should be continued. It is also unclear whether CLRT should be started at full rotation immediately or begun at lesser degrees of rotation and advanced serially over several hours. Another unknown is the minimum time that CLRT should be administered per day. In the studies discussed, most patients were rotated for 10 to 16 h/day. The minimum degree of rotation necessary for an effect is also unknown; in the studies cited, rotations from 40 degrees to 62 degrees in each direction were used. Based on the current data, the early use of CLRT in comatose or otherwise immobile patients decreases the incidence of LRTI including pneumonia over the first 7 to 14 days of ICU care. The prevention of pneumonia and more rapid transfer from the ICU should offset the additional expense of a specialized bed. The data suggest that a multicenter study with accrual of a large number of patients to evaluate this form of therapy in a prospective, randomized study is necessary. If the hypothesis that CLRT decreases the incidence of nosocomial pneumonia in the ICU is proven, the impact on critical care in the 90s would be substantial.
Beds↗
Management of parapneumonic pleural effusions and empyema.
Parapneumonic pleural effusions, the most common causes of exudative pleural fluid, are a frequent finding with bacterial pneumonia. Progression to empyema is related to delay in appropriate antimicrobial therapy. Once an empyema develops, therapy consists of early sterilization of the empyema space with appropriate antibiotics, early and adequate pleural space drainage, and obliteration of the empyema cavity by adequate lung expansion, surgical decortication, or enzymatic debridement.
Empyema, Pleural↗
Thoracentesis: a safe procedure in mechanically ventilated patients.
Explore the source record for details and available documents.
Adolescent↗
Subglottic stenosis in Wegener's granulomatosis: development during cyclophosphamide treatment with response to carbon dioxide laser therapy.
A patient with Wegener's granulomatosis rapidly developed a circumferential subglottic stenosis while on a cyclophosphamide regimen that had caused resolution of systemic symptoms and pulmonary infiltrates. The stenosis developed in the area of previously noted tracheal ulceration and responded satisfactorily to carbon dioxide laser therapy.
Adult↗
The pathophysiology of pleural effusions.
Two features of human parietal pleura explain its role in the formation and removal of pleural liquid and protein in the normal state: the proximity of the microvessels to the pleural surface and the presence of stomata situated between mesothelial cells. For pleural fluid to accumulate in disease, there must be increased production from increased hydrostatic pressure, decreased oncotic or pleural pressure, increased microvascular permeability, or peritoneal-pleural movement. The rate of formation must overwhelm lymphatic clearance, which may be decreased by hydrostatic forces or blocked by malignant infiltration.
Animals↗
Mechanical ventilation.
Among the many advances made in intensive care therapeutics in recent years, few have rivaled the impact of mechanical ventilators. Their expanded use affects all who practice in the critical care setting. This article reviews the physiologic basis for mechanical ventilation, how ventilators are classified, the various modes, and specific indications. A basic introduction is made into ventilator set up, weaning techniques, adjunctive drug therapy, and complications. The pharmacotherapy specialist who understands interactions between patients and ventilators, and the effects of mechanical ventilation on cardiopulmonary function will be best equipped to individualize drug therapy.
Critical Care↗
Medical management and therapy of bronchopleural fistulas in the mechanically ventilated patient.
Bronchopleural fistulas are associated with high morbidity and mortality and are particularly challenging in the ventilated patient. Familiarity with both basic and more technical medical management techniques may lessen morbidity and improve survival. Prompt recognition of BPFs and appropriate placement of a chest tube with an adequate suction device are crucial to prevent potential tension pneumothorax and to drain an infected pleural space. The chest tube may be used therapeutically to decrease BPF air leak and to promote fistula repair. Appropriate conventional ventilator manipulations aimed at decreasing fistula air leak and maintaining adequate oxygenation and ventilation may fail and necessitate a trial of HFV. Definitive therapy by the bronchoscopic application of a sealing agent to occlude the fistula site can be used, particularly in the poor surgical candidate.
Bronchial Fistula↗
Sarcoidosis presenting as progressive ascending lower extremity weakness and asymptomatic meningitis with hypoglycorrhachia.
A 26-year-old man developed progressive weakness over a two-month period. His chest radiograph showed diffuse interstitial infiltrates, and transbronchial lung biopsies demonstrated noncaseating granulomas consistent with sarcoidosis. Sarcoid neuropathy should be considered in the differential diagnosis of the patient presenting with an atypical Landry-Guillain-Barré syndrome.
Adult↗
Acid-base disturbances in acute asthma.
The clinical features, arterial blood gases, and acid-base profile were examined in 229 consecutive episodes of acute asthma in 170 patients who required hospitalization. A simple respiratory alkalosis was the most common acid-base disturbance, occurring in 48 percent of the episodes. Metabolic acidosis, either alone or as part of a mixed disturbance, was noted in 28 percent. Of 60 episodes presenting with respiratory acidosis, 37 (62 percent) had a coexistent metabolic acidosis. Metabolic acidosis was more likely to occur in male subjects and in patients with evidence of more severe airflow obstruction. Patients with metabolic acidosis had an average anion gap of 15.8 mEq/L; these patients were more hypoxemic than those without metabolic acidosis and there was a significant inverse correlation between the anion gap and the degree of hypoxemia. We conclude that metabolic acidosis is a common finding in acute, severe asthma and suggest that the pathogenesis of lactic acidosis is multifactorial and includes contributions from lactate production by respiratory muscles, tissue hypoxia, and intracellular alkalosis.
Acid-Base Equilibrium↗
Hypothyroidism and pleural effusions.
Serous effusions have been thought to be an unusual complication of hypothyroidism and most commonly have been associated with ascites, pericardial fluid and heart failure. Pleural fluid as an isolated finding in hypothyroidism is apparently rare and complete analysis of these hypothyroid-associated pleural effusions has not been described. To determine the frequency, chemical characteristics and clinical associations of hypothyroidism and pleural effusions, the medical records of 128 patients with hypothyroidism (defined by an increased serum TSH concentration) were reviewed. The majority of effusions in patients with hypothyroidism were due to other diseases. Effusions solely due to hypothyroidism appeared to be a real entity. These effusions were borderline between exudates and transudates and showed little evidence of inflammation.
Aged↗
Do chest radiographic findings reflect the clinical course of patients with sarcoidosis during corticosteroid withdrawal?
The use of serial chest radiographs to assess disease activity in patients with sarcoidosis is controversial. However, reliance on the symptomatic clinical course to assess disease activity may be misleading. As many patients being treated with corticosteroids have an abrupt clinical deterioration when doses of those medications are decreased, we questioned whether the chest radiograph could depict alterations in disease activity as measured by spirometry in this subset of patients. We retrospectively reviewed the clinical course of all patients with pulmonary sarcoidosis in whom the corticosteroid dose was reduced during a 6-month period. The 15 patients without fever, chills, or purulent sputum during that time were then examined to determine the presence (n = 10) or absence (n = 5) of a symptomatic relapse. All patients who had a symptomatic relapse also had a fall in forced vital capacity of at least 10%, suggesting an increase in disease activity. Serial chest radiographs were evaluated during and after corticosteroid dose reductions and after clinical recovery on higher steroid doses in the patients who had had a relapse. In eight patients, the disease was in radiographic stage 2 (hilar adenopathy and parenchymal lung disease); in seven patients it was in radiographic stage 3 (parenchymal lung disease alone). The disease did not change stage in any patient during the study. Chest radiographs worsened more frequently in patients who had a clinical relapse (seven of 10) than in those who did not have a relapse (zero of five, p less than .05). An alveolar chest radiographic pattern (n = 4) or reticulonodular pattern (n = 3) was noted in the seven patients who had a relapse, with worsening on radiographs often occurring before detection of relapse by symptomatology (four of seven) or spirometry (three of seven). Spirometry and radiographs improved or stabilized after an increase in corticosteroid dose in all 10 patients who had a relapse. We conclude that serial chest radiographs can reflect clinical relapse in patients with sarcoidosis during corticosteroid dose reduction. Furthermore, worsening seen on chest radiographs may be the first evidence of relapse.
Adrenal Cortex Hormones↗
The histology of experimental pleural injury with tetracycline, empyema, and carrageenan.
Models of pleural injury were established with intrapleural tetracycline, intrapleural carrageenan, and empyema in New Zealand White rabbits to evaluate histologically the pleural inflammatory response from 3 to 90 days. Both tetracycline and empyema models produced increases in the pleural connective tissue layers both above and below the fibroelastic membrane associated with angiogenesis and lymphangiogenesis. The influx of fibroblasts from the pleural surface into acellular fibrin strands formed adhesions between the visceral and the parietal pleurae. Injury to the mesothelial cell ranged from a cuboidal transition to total desquamation with the degree of mesothelial injury associated with the amount of fibrin adherence and the propensity toward fibrosis at 90 days. Intervention to promote the resolution of pleural inflammation without fibrosis should be directed toward preservation of the mesothelial surface, removal of pleural fibrin, and inhibition of fibroblast growth and chemotaxis.
Animals↗
Pleural effusions associated with ethchlorvynol lung injury result from visceral pleural leak.
Traditional thinking suggests that pleural fluid develops on the basis of systemic venous hypertension or a primary pleural process. Recent investigations, however, indicate that both acute lung injury and pulmonary venous hypertension can be important in the pathogenesis of pleural effusions. To evaluate the role of acute lung injury in the formation of pleural effusions, we developed a model of acute, reversible lung injury in NZW rabbits. Intravenous ethchlorvynol (ECV), known to produce permeability edema in humans, was used to produce permeability pulmonary edema in rabbits. The injury was examined over 14 days with bronchoalveolar lavage, pleural fluid analysis, and morphologic analysis. Ethchlorvynol injection (40 mg/kg) produced a PMN-predominant, exudative alveolitis (2 h), alveolar hemorrhage (6 to 10 h), and pleural effusions by 2 h (peak, 10 h). Pathologic findings included a patchy, subpleural, hemorrhagic PMN inflammatory response, which peaked by 24 h, and an acute PMN vasculitis of small arterioles and capillaries; these changes resolved in 5 to 7 days. No parietal pleural abnormalities were observed. We conclude that ECV induces an acute, reversible parenchymal lung injury resulting in a capillary leak and that fluid moves from the interstitium of the lung into the pleural space along a pressure gradient through a relatively permeable mesothelium. The data support the concept that diffuse or localized lung injury can result in pleural effusions.
Acute Disease↗
Bilateral exudative pleural effusions following intravenous ethchlorvynol administration.
A 26-year-old man had bilateral alveolar infiltrates and exudative pleural effusions following self-administration of intravenous ethchlorvynol (ECV). The effusions and pulmonary edema resolved by 72 h with supportive therapy only. As no other etiology was established, we concluded that the pathogenesis of the pleural fluid was the transvisceral pleural leak of the increased extravascular lung water induced by ECV. Current experimental and clinical evidence support the concept that pleural effusions probably develop in most states of permeability pulmonary edema.
Adult↗