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J W Leatherman

Publications and source records attributed to J W Leatherman.

18 recordsLinked to original sources
PubMed1992

Intrapleurally administered streptokinase in the treatment of acute loculated nonpurulent parapneumonic effusions.

Adequate pleural drainage is believed to be an essential component of the management of low pH-low glucose parapneumonic effusion. Parapneumonic effusions may become loculated rapidly, preventing adequate drainage with a single chest tube. Administration of intrapleural streptokinase may be effective in promoting drainage for loculated, nonpurulent low pH-low glucose parapneumonic effusions when fibrin adhesions may not yet be organized. Intrapleural streptokinase was used in 12 patients with relatively large, symptomatic, loculated, nonpurulent parapneumonic effusions in whom the initial thoracentesis demonstrated a pH less than or equal to 7.0 and/or glucose less than or equal to 40 mg/dl, and when inadequate drainage was demonstrated roentgenographically despite tube thoracostomy. Mean pleural fluid WBC was 9,750/mm3 (range, 1 to 27 K), and pleural fluid glucose and pH were 33 +/- 21 mg/dl and 6.95 +/- 0.19, respectively. A solution of streptokinase, 250,000 units in normal saline, was given intrapleurally via the chest tube. Effectiveness of intrapleural streptokinase was assessed radiographically and by monitoring the volume of fluid drained from the chest tube after streptokinase instillation. A greater than 50% improvement in the CXR was seen in nine of 12 patients after intrapleural administration of streptokinase. The volume of fluid out in the first 48 h post-streptokinase was 849 +/- 836 ml (range, 100 to 3,000). In addition, clinical improvement (decreased chest discomfort, less dyspnea, or reduced fever) was noted in eight of 12 patients after streptokinase treatment. We conclude that intrapleural administration of streptokinase is an effective adjunct to the management of nonpurulent, loculated parapneumonic effusions that may reduce the need for multiple chest tubes or surgical drainage.

Acute Disease↗
PubMed1992

Intracardiac mural thrombus mimicking atrial myxoma in the antiphospholipid syndrome.

A wide spectrum of cardiac involvement including valvular lesions, myocardial infarction and myocardial dysfunction has been reported in patients with antiphospholipid antibodies (aPL), suggesting that cardiac manifestations may be part of the antiphospholipid syndrome (APS). We describe 3 patients (2 with primary APS and one with APS and SLE) who were found to have right atrial masses by echocardiography (transthoracic and/or transesophageal) and/or angiography, which were felt preoperatively to be atrial myxomata. Pathological examination of resected material showed only organized thrombus with calcification. We describe outcome 12 months to 7 years after resection of thrombus and document possible recurrence in one patient after 7 years. Intracardiac mural thrombus may be an additional cardiac manifestation of the APS, and presents considerable diagnostic confusion in its differentiation from atrial myxomata.

Adolescent↗
PubMed1991

Fever, hyperdynamic shock, and multiple-system organ failure. A pseudo-sepsis syndrome associated with chronic salicylate intoxication.

OBJECTIVE: To describe a sepsis-like syndrome associated with chronic salicylate intoxication. DESIGN: Retrospective clinical study. SETTING: University-affiliated county hospital. PATIENTS: Five patients who became accidentally intoxicated while ingesting salicylates on a long-term daily basis. RESULTS OF DATA ANALYSIS: All five salicylate-intoxicated patients had clinical and laboratory features that were highly suggestive of sepsis, but no bacteriologic or pathologic evidence of infection could be documented. Features included fever, leukocytosis with increased band forms, hypotension with a reduced SVR and multiple system organ failure (ARDS, encephalopathy, renal failure, and DIC). A diagnosis of salicylate intoxication was made at the time of admission to the hospital in only one case. In the other four cases, the presumptive diagnosis was sepsis; a correct diagnosis of salicylate intoxication was not established until between 16 h and 10 days after admission in these four cases. Two patients died, one patient required permanent hemodialysis, and two patients recovered fully only after prolonged and complicated hospitalizations. The pathogenesis of this syndrome is uncertain. In two cases, serum levels of TNF-alpha, IL-1 beta and IL-6 were measured by ELISA. In both cases serum IL-6 was markedly increased, and in one case serum TNF-alpha was also elevated. CONCLUSION: Occult salicylate intoxication should be considered when apparent sepsis syndrome occurs without a readily easily identifiable source of infection.

Adult↗
PubMed1991

Tidal volume reduction in ARDS. Effect on cardiac output and arterial oxygenation.

During continuous positive pressure ventilation (CPPV), mean airway pressure and lung volume will be influenced both by the tidal volume (VT) employed and the amount of positive end-expiratory pressure (PEEP). The effect of varying levels of CPPV on PaO2 and cardiac output (Q) has been previously assessed by adjusting the level of PEEP at constant VT. This study examined the influence of a 200-ml reduction in VT, at a constant PEEP of 15 cm H2O, on the PaO2 and Q of 21 patients with adult respiratory distress syndrome (ARDS). The relationship between change in Q and change in total respiratory system compliance (Cst) after VT reduction was also examined. VT reduction from 14.1 +/- 0.8 ml/kg to 11.2 +/- 0.9 ml/kg yielded an increase in Q (+ 15 +/- 12 percent, p less than 0.01) without a significant change in PaO2 (-6.3 +/- 15.0 mm Hg, p = 0.08). Cst increased with VT reduction (+ 3.1 +/- 1.8 ml/cm H2O). There was only a modest correlation (r = +0.42, p = 0.06) between delta Q percent and delta Cst following VT reduction. VT reduction at high level PEEP may yield a significant improvement in Q and net O2 delivery, but the degree of hemodynamic improvement is variable and is not reliably predicted noninvasively by measurement of Cst.

Adult↗
PubMed1988

The lung in systemic vasculitis.

Pulmonary vasculitis is usually caused by one of three disorders: (1) Wegener's granulomatosis (WG); (2) Churg-Strauss syndrome (CSS), or allergic angiitis and granulomatosis; or (3) a nonspecific small vessel systemic necrotizing vasculitis (SNV), or microscopic polyarteritis. WG, the most common cause of lung vasculitis, has features of a granulomatous vasculitis of the upper airway and lung and widespread small vessel vasculitis involving the kidneys and other organs. The features of pulmonary WG overlap with those of malignancy and infectious granulomatous lung disease; accurate diagnosis generally requires open lung biopsy. CSS is defined by the triad of asthma, eosinophilia, and systemic vasculitis. Easily accessible tissues should be biopsied, but the clinical features are so distinctive that tissue biopsy is not invariably required for diagnosis. CSS must be differentiated from other diseases that cause pulmonary infiltrates with eosinophilia, including infections. Nonspecific SNV causes diffuse alveolar hemorrhage due to pulmonary capillaritis. Concomitant segmental necrotizing glomerulonephritis is almost always present. Diagnosis is made by renal biopsy, compatible extrarenal features, exclusion of nonimmune causes of lung hemorrhage, and exclusion of WG to the extent possible.

Churg-Strauss Syndrome↗
PubMed1988

Respiratory manifestations of connective tissue disease.

Pleuropulmonary disease is a common feature of the following connective tissue diseases: systemic lupus erythematosis (SLE), rheumatoid arthritis (RA), progressive systemic sclerosis (PSS), mixed connective tissue disease (MCTD), polymyositis/dermatomyositis (PM/DM), and Sjogren's syndrome (SS). Features common to most of these disorders include pleurisy with effusion and interstitial lung disease. Pleural effusions caused by SLE and RA have certain characteristics on pleural fluid analysis that aid in diagnosis, but infection and other causes of effusion must be excluded. Interstitial lung involvement is usually indolent in onset, but a more rapidly progressive course over weeks to a few months may mimic infection. Several drugs used to treat connective tissue diseases may cause interstitial disease, increase susceptibility to infection, or both. This complicates differential diagnosis. Acute lupus pneumonitis and SLE-related alveolar hemorrhage are usually fulminant processes, often associated with fever. Diagnosis of these conditions always requires exclusion of infection. Rheumatoid nodules may mimic infectious and neoplastic lung diseases. Needle biopsy helps reduce the likelihood of infection or malignancy, but open lung biopsy is needed if a firm diagnosis of rheumatoid nodules is required.

Arthritis, Rheumatoid↗
PubMed1987

Aminophylline for acute exacerbations of chronic obstructive pulmonary disease. A controlled trial.

STUDY OBJECTIVE: To determine the efficacy of intravenous aminophylline in the treatment of patients hospitalized for exacerbation of chronic obstructive pulmonary disease. DESIGN: Randomized, double-blind, placebo-controlled trial during the first 72 hours of hospitalization. PATIENTS: Thirty patients admitted from the emergency room or walk-in clinic with the primary diagnosis of an exacerbation of chronic obstructive pulmonary disease. Twenty-eight patients completed the study; 2 patients, 1 receiving placebo and 1 receiving aminophylline, were removed from the study because of respiratory failure requiring mechanical ventilation. INTERVENTIONS: PATIENTS received either intravenous aminophylline or placebo, in addition to nebulized, inhaled 0.3 mL of a 5% solution every 6 hours; methylprednisolone, 0.5 mg/kg body weight every 6 hours intravenously; ampicillin, 500 mg orally every 6 hours (tetracycline or trimethoprim-sulfamethoxazole were substituted in penicillin-allergic patients); and supplemental oxygen as needed. Aminophylline infusion rates were adjusted by an unblinded investigator to achieve theophylline levels of 72 to 83 mumol/L. Changes were also made in placebo infusion rates to maintain the double-blind design. MEASUREMENTS AND MAIN RESULTS: The forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) before and after metaproterenol inhalation were measured twice daily by a blinded investigator, who also administered a verbal dyspnea index with a scale of 1 to 10 and questioned patients regarding possible side effects of treatment (tremor, palpitations, nausea, or vomiting). Arterial blood gas measurements at 72 hours were compared with those obtained on admission. Significant improvements in FEV1 and FVC measured before and after metaproterenol treatment and in dyspnea occurred over time in both treatment groups (p less than 0.05 for all measurements). However, there were no significant differences between the placebo and aminophylline groups in any of the spirometric measurements or the dyspnea indices (p greater than 0.5 in all five analyses). The mean increases (+/- SE) in Po2 of 1.9 (+/- 0.5) kPa with placebo and 1.7 (+/- 0.7) kPa with aminophylline and the mean decreases in PCO2 of 0.5 (+/- 0.4) kPa with placebo and 1.2 (+/- 0.4) kPa with aminophylline were not significantly different (p greater than 0.6 for PO2, p greater than 0.2 for PCO2).(ABSTRACT TRUNCATED AT 400 WORDS)

Acute Disease↗
PubMed1985

Fluid-containing bullae in the lung.

Eight patients had air-fluid levels in the lung as a result of fluid accumulation in preexisting bullae. In four cases the cause was peribullous pneumonitis; in the other four cases the cause could not be determined. All patients had a favorable clinical course while intrabullous fluid was present. The initial interpretation of air-fluid levels was correct in only two instances. Differentiation of fluid-containing bullae from other causes of air-fluid levels is important so that unnecessary diagnostic and therapeutic maneuvers can be avoided.

Aged↗
PubMed1984

Lung T cells in hypersensitivity pneumonitis.

Monoclonal antibodies OKT3 (all T cells), OKT4 (T-helper/inducer), and OKT8 (T-suppressor/cytotoxic) were used to determine surface phenotypes of bronchoalveolar lavage and peripheral blood lymphocytes in patients with chronic hypersensitivity pneumonitis. Similar studies were done in asymptomatic pigeon breeders, patients with sarcoidosis, and nonsmoking controls. Increased numbers of lavage T cells were found in patients with hypersensitivity pneumonitis and sarcoidosis and in asymptomatic pigeon breeders. The predominant T-cell subset in patients with hypersensitivity pneumonitis and in asymptomatic pigeon breeders was T8 +; in contrast, the predominant subset in those with sarcoidosis was T4 +. Peripheral blood T-cell subsets were normal in all groups. Thus, most lung T lymphocytes in chronic hypersensitivity pneumonitis belong to the T8 + subset; the local cellular immune response in hypersensitivity pneumonitis and sarcoidosis are different; and the pattern of alveolitis, as determined by bronchoalveolar lavage, is not the sole determinant of lung impairment after exposure to hypersensitivity pneumonitis antigens.

Adult↗
PubMed1984

Alveolar hemorrhage syndromes: diffuse microvascular lung hemorrhage in immune and idiopathic disorders.

We have reviewed the alveolar hemorrhage (AH) syndromes, defined as immune or idiopathic disorders associated with diffuse microvascular hemorrhage into the acinar portion of the lung. The disorders that are most often associated with AH include antibasement membrane antibodies (ABMA) disease, idiopathic pulmonary hemosiderosis, systemic lupus erythematosus, systemic vasculitides, and idiopathic rapidly progressive glomerulonephritis. An approach to the recognition, diagnosis, and treatment of the AH syndromes has been outlined and several illustrative case studies have been presented. Recognition of AH is not usually difficult, but does require a high index of suspicion, since many disease processes may give rise to hemoptysis with infiltrates on chest roentgenogram. Recognition of AH is aided by careful clinical and laboratory assessment for evidence of extrapulmonary disease; simple hematologic studies such as sequential hemoglobins and iron studies; and measurement of carbon monoxide uptake by the lungs. Early recognition of AH may decrease the likelihood of respiratory failure and end-stage renal disease. The specific etiology of AH is usually determined by clinical examination, serologic assay for ABMA, and percutaneous renal biopsy by immunofluorescence. Open-lung biopsy is required in a minority of cases. High-dose pulse methylprednisolone appears to effectively control AH of diverse etiology. Combined plasma exchange and immunosuppression controls AH in ABMA disease and is the treatment of choice in this disorder. Cyclophosphamide is used for Wegener's granulomatosis, and sometimes in systemic necrotizing vasculitis, in an attempt to prevent irreversible damage to the kidneys.

Adult↗
PubMed1984

Cavitation in bacteremic pneumococcal pneumonia. Causal role of mixed infection with anaerobic bacteria.

Cavitation developed in 4 of 24 patients with bacteremic pneumococcal pneumonia seen in 1 yr. Two of them had roentgenographic evidence of massive pulmonary gangrene. A total of 3 patients developed putrid sputum at the time of cavitation, proving that anaerobes were present. Culture confirmation of anaerobic etiology (Bacteroides fragilis) was obtained in 1 patient who had a thoracotomy for pulmonary gangrene. Putrid sputum was observed only in cavitary cases. Other clinical and epidemiologic features (bilateral infiltrates, alcoholism), which were more frequent in cavitary than in noncavitary cases, are often associated with anaerobic infection. These findings support the hypothesis that concomitant anaerobic infection may be responsible for cavitation in bacteremic pneumococcal pneumonia.

Adult↗
PubMed1983

Pulmonary edema due to upper airway obstruction.

We have reported a case of severe upper airway obstruction accompanied by marked inspiratory effort which produced highly negative intrathoracic pressure, leading to a reduction in pulmonary interstitial hydrostatic pressure and impairment of left ventricular performance. Acute pulmonary edema resulted. Severe acidosis was also present and may have contributed to left ventricular dysfunction.

Acidosis↗
PubMed1982

Diffuse intrapulmonary hemorrhage and glomerulonephritis unrelated to anti-glomerular basement membrane antibody.

Nine patients with diffuse intrapulmonary hemorrhage and glomerulonephritis not due to anti-glomerular basement membrane (anti-GBM) antibody are described and similar previously reported cases are reviewed. Eight patients were seen during a four-year interval and represented 47 percent of the cases of pulmonary hemorrhage and glomerulonephritis seen during this period. Diagnoses included systemic vasculitis of unspecified type in two patients with seropositive rhematoid arthritis, idiopathic crescentic glomerulonephritis with negative immunofluorescence in two, Wegener's granulomatosis in two, and polyarteritis nodosa, Henoch-Schönlein purpura, and mixed connective tissue disease in one each. Differentiation from anti-GBM antibody-mediated pulmonary hemorrhage and glomerulonephritis by clinical evaluation alone was frequently difficult, emphasizing the importance of both immunopathologic studies and evaluation of serum for anti-GBM antibody in all patients with pulmonary hemorrhage and glomerulonephritis. In eight of nine patients, significant episodes of pulmonary hemorrhage improved markedly within 24 to 72 hours following initiation of high-dose corticosteroid therapy. In contrast, renal function did not improve in the majority of patients.

Adult↗
PubMed1979

Vasopressin-resistant nephrogenic diabetes insipidus. A result of amphotericin B therapy.

Polyuria and polydipsia developed in two cases during amphotericin B therapy for deep mycoses. Neither patient could concentrate his urine in response to water deprivation or exogenous vasopressin. Other causes of vasopressin-resistant nephrogenic diabetes insipidus were not present. Three months after amphotericin B therapy had been discontinued, concentrating ability improved toward normal. A third patient was further observed and demonstrated normal diluting capacity but impaired free-water reabsorption, suggesting a distal tubular defect consistent with nephrogenic diabetes insipidus. Four months after discontinuing therapy, renal concentrating ability was normal. Amphotericin B can induce a reversible form of nephrogenic diabetes insipidus.

Amphotericin B↗