Although commonly found at autopsy, leukemic infiltration of the lung is rarely recognized as a cause of respiratory symptoms or roentgenographic densities. Previously reported cases of patients who had symptomatic or roentgenographic acute leukemic lung diseases invariably presented with diffuse pulmonary infiltrates. We describe three patients with leukemic involvement of the lung who presented with cough, fever, and localized roentgenographic infiltrates suggestive of bacterial pneumonia. In each case, the diagnosis was made by transbronchial biopsy specimen and confirmed by complete response to chemotherapy. In common with the other reported cases, all of our patients had peripheral blast counts above 40 percent (greater than 6,000 blasts per ml3) at the time the pulmonary diagnosis was made. Leukemic invasion of the lung should be considered in patients with acute leukemia who develop lung infiltrates--whether diffuse or focal--in association with a high peripheral blast count.

Chronic bronchitis is characterized by mucociliary dysfunction resulting from structural and functional defects of cilia and the secretory apparatus. The combination of hypersecretion and ciliary impairment leads to disruption of mucociliary interaction and hence the accumulation of secretions in the lower airways. Cigarette smoke appears to play a critical role in the pathogenesis of chronic bronchitis-associated mucociliary dysfunction. While the excessive lower airway secretions may have only minor effects on the natural course of airflow obstruction, they could transiently compromise airway function during acute exacerbations. In addition, altered aerosol deposition in the airways resulting from excessive airway secretions could influence the airway responses to inhaled irritants and pharmacologic agents. There are currently no direct, non-invasive methods available to assess the quantity and distribution of airway secretions in vivo. Indirect indices such as cough frequency, sputum volume, respiratory function, and mucociliary clearance are nonspecific and subject to misinterpretation. The clinical utility of mucotropic pharmacologic agents and of physical maneuvers directed at removing excessive lower airway secretions is therefore difficult to evaluate objectively.

Cheyne-Stokes respiration is characterized by crescendo-decrescendo fluctuations in tidal volume and respiratory rate interrupted by central apneas. It has long been associated with cardiac disease and has often been cited as a poor prognostic indicator, yet the incidence and immediate significance of CSR in the setting of acute cardiogenic PE is not well defined. Therefore, we studied 95 patients who required MVS because of PE. Breathing patterns were monitored by continuous respiratory inductive plethysmography for a minimum of 12 hours of spontaneous respiration after recovery from PE; CSR was noted in 42 patients (44 percent). There were no significant differences between patients with PE and CSR and those with only PE in regard to LVEF (mean +/- SD, 36 +/- 18 percent vs 33 +/- 16 percent; p = 0.55), reinstitution of MVS within 48 hours (4.8 percent vs 17.0 percent; p = 0.065), or in-hospital mortality (16.7 percent vs 26.4 percent; p = 0.255). We conclude that CSR is a relatively common breathing pattern in patients who required MVS because of cardiogenic PE and does not portend a poor immediate prognosis in this population.

Carbon monoxide poisoning is a major cause of illness and death in the United States. Most cases result from exposure to the internal combustion engine and to stoves burning fossil fuels. Most cases of accidental exposure are preventable if proper precautions are taken; however, when cases arise, their presenting signs and symptoms are nonspecific and often lead to a misdiagnosis resembling a flu-like viral illness. As a result, the incidence of acute CO poisoning is underestimated. The effects of CO poisoning are due to tissue hypoxia, with the CNS and the heart being the most susceptible target organs due to their high oxygen needs. Prolonged hypoxia due to high CO levels may lead to cardiac arrhythmias or arrest (or both) and a variety of neurologic sequelae. Treatment is directed toward the relief of tissue hypoxia and the removal of CO from the body. Severity of poisoning can be divided into three levels based on CO levels in the blood. Administration of normobaric 100 percent oxygen is the therapy of choice for most cases, while hyperbaric oxygen therapy is reserved for severe poisonings.

Silent ischemia is a common finding in coronary artery disease and occurs more frequently than painful episodes in the total ischemic burden. Since painless ischemia places limits on the history, it can encourage physicians to spend more time studying and treating the electrocardiogram and less time with patients, potentially leading to a deterioration in doctor-patient relationship and care. Silent ischemia should be considered only in patients 35 years of age or older who: (a) have a strong family history of early coronary artery disease, or (b) have two major coronary risk factors. Verification is made by performing an electrocardiographic exercise stress test and followed by a thallium-201 electrocardiographic stress test when the electrocardiograms are equivocal. In females it is best to proceed directly to a thallium-201 electrocardiographic stress test because of the frequency of false positives on the exercise electrocardiograms. The results will help determine the indications for further studies and subsequently the need for drug or interventional management. Frequently a history in which symptoms of lower esophageal disorders, hiatal hernia, gastric disease and arthritic pains mimic angina or in fact coexist with ischemic heart disease makes the clinical diagnosis of angina more elusive and difficult. However, a careful unhurried history and an exercise stress test can often differentiate the etiology of the chest pains. A 24-hour ambulatory electrocardiographic recording aids in measuring the total ischemic burden. When the diagnosis and severity of the ischemic syndrome is established, a course of medical therapy tailored to the symptoms and with defined end points is initiated. Since silent ischemia and angina frequently coexist, suppression of the frequency and severity of the anginal episodes will also reduce the episodes of silent ischemia. Symptomatic improvement is thus a guide in the treatment of the total ischemic syndrome. Drug management will usually consist of two or more of the following drugs: a nitrate, beta blocker, calcium channel blocker, and aspirin. A 24-hour ambulatory electrocardiographic recording is helpful in assessing the efficacy of medical management of silent ischemia. Failures in drug management should proceed with coronary angiography, and when indicated, followed by percutaneous transluminal coronary angioplasty or coronary artery bypass graft surgery.

The pharmacodynamics and pharmacokinetics of beta-lactam antibiotics in patients with cystic fibrosis are discussed. A hypothetical dosing regimen based on these principles is considered. The usual dosing regimens may be suboptimal. New dosage regimens should be studied using prospective, controlled, randomized and blinded clinical trials.

The chest x-ray film a 22-year-old man showed a large right-sided pleural effusion that was grossly hemorrhagic when aspirated. A computerized tomographic scan showed a complex mass with cystic components contiguous with the diaphragm. On thoracotomy the mass was found to be arising from the diaphragm and had the consistency of an organizing hematoma. Pathologic studies showed the mass to be an epithelioid hemangioendothelioma. This rare tumor has never been reported previously as arising from the diaphragm. It has a variable prognosis, but surgery remains the treatment of choice. In this report, we review the clinical and pathologic characteristics of this unusual tumor, as well as the distinctive roentgenographic findings with which it presented.

There is now incontrovertible evidence that there is a progressive and strikingly increased mortality from bronchial asthma in the US. The increase is more dramatic in the older age groups, but younger age groups are not spared. The exact cause or causes of this increased mortality are not known, and it is even possible (although not likely) that the increase is artifactual. This increased death rate is in sharp contrast to the general medical perception that major advances in the management of bronchial asthma have occurred. Perhaps they have, but if so, more patients are dying during this period of advances than were dying before. The most prudent course would be to assume that the excess deaths are iatrogenic in origin and to act accordingly. Even if this assumption is flawed, acting on it would improve the management of patients with bronchial asthma. If it is true that the major purpose of risk-benefit analysis is to improve patient outcome rather than merely analyze risk-benefit balance, then a series of proposals can be generated to grapple with this problem in bronchial asthma.

The possible contribution of computed tomography (CT) in the management of patients with solitary pulmonary nodules (SPNs) or masses was reviewed retrospectively in 65 patients undergoing fiberoptic bronchoscopy (FOB). Nodules were evaluated by size, location, surface contour, and the presence in cross-section of a bronchus leading to or contained within the nodule or mass, a "positive bronchus sign." Thirty-five lesions were associated with a positive bronchus sign; 21 of 35 (60 percent) were diagnosed endoscopically, (p = .027); of 30 cases with a negative bronchus sign, only ten (30 percent) had a diagnosis made by FOB (p = .034). It is concluded that CT may be of use in the routine evaluation of pulmonary nodules, prior to bronchoscopy, especially in cases for which histologic evaluation is essential, especially to determine the presence or absence of a CT bronchus sign.

To evaluate available clinical methods (self ratings and questionnaire) for rating dyspnea, we (1) compared scores from the recently developed baseline dyspnea index (BDI) with the Medical Research Council (MRC) scale and the oxygen-cost diagram (OCD) in 153 patients with various respiratory diseases who sought medical care for shortness of breath; and (2) evaluated the relationships between dyspnea scores and standard measures of physiologic lung function in the same patients. The dyspnea scores were all significantly correlated (r = 0.48 to 0.70; p less than 0.001). Agreement between two observers or with repeated use was satisfactory with all three clinical rating methods. The BDI showed the highest correlations with physiologic measurements. Dyspnea scores were most highly related to spirometric values (r = 0.78; p less than 0.001) for patients with asthma, maximal respiratory pressures (r = 0.34 and 0.35; p less than 0.001) for patients with chronic obstructive pulmonary disease, and PImax (r = 0.51; p = 0.01) and FVC (r = 0.44; p = 0.03) for those with interstitial lung disease. These results show that: (1) the BDI, MRC scale, and OCD provide significantly related measures of dyspnea; (2) the clinical ratings of dyspnea correlate significantly with physiologic parameters of lung function; and (3) breathlessness may be related to the pathophysiology of the specific respiratory disease. The clinical rating of dyspnea may provide quantitative information complementary to measurements of lung function.