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Biomedical subjects

J E Heffner

Publications and source records attributed to J E Heffner.

At least 109 records · Page 6Linked to original sources
PubMed1987

Sarcoid-like hilar and mediastinal lymphadenopathy in a patient with metastatic testicular cancer.

Previous reports indicate that enlarged hilar and mediastinal lymph nodes due to sarcoid-like reactions may develop after curative resection of testicular cancer, and their presence does not necessarily denote neoplastic recurrence. Reports further suggest that coexisting pulmonary nodules in this setting may be related to nodular sarcoidosis. A patient developed progressive hilar and mediastinal adenopathy associated with multiple pulmonary nodules after apparent curative resection of a testicular embryonal cell cancer. Biopsy specimens from the mediastinal lymph nodes demonstrated granulomas, suggesting the diagnosis of nodular sarcoidosis. Needle aspiration of the pulmonary nodules, however, revealed metastatic testis cancer. Sarcoid-like mediastinal reactions occur after resection of testis cancer, but biopsies should be performed on coexisting pulmonary nodules to exclude pulmonary metastases.

Adult↗
PubMed1987

Pulmonary hemorrhage and air embolism complicating transbronchial biopsy in pulmonary amyloidosis.

We describe a fatal complication of transbronchial biopsy in a patient with pulmonary parenchymal amyloidosis. Hemorrhage after biopsy required intubation and positive-pressure ventilation that resulted in massive arterial air embolism. Postmortem findings suggested that the bleeding and air embolism were related to persistent patency of biopsied blood vessels infiltrated with amyloid. Patients with pulmonary amyloidosis may be at increased risk of major complications after transbronchial biopsy.

Aged↗
PubMed1984

Staphylococcus aureus and human platelets cause pulmonary hypertension and thromboxane generation in isolated saline-perfused rabbit lungs.

The potential contributions of bacterial-platelet interactions to the development of acute edematous lung injury, such as that seen in the adult respiratory distress syndrome (ARDS), remains unknown. We found that the addition of Staphylococcus aureus, 502A to isolated rabbit lungs perfused with saline, and human platelets rapidly decreased the number of circulating platelets, increased pulmonary artery perfusion pressures, and generated thromboxane B2, the stable derivative of thromboxane A2. In contrast, increases in perfusion pressures or thromboxane levels did not occur when platelets treated with acetylsalicylic acid (ASA) were used, even though ASA-treated platelets disappeared from the perfusates. The results suggest that activation of platelets by bacteria may account for thrombocytopenia, platelet microemboli, and/or contribute to increases in pulmonary artery pressures seen in some patients with ARDS.

Animals↗
PubMed1983

Acetyl glyceryl ether phosphorylcholine-stimulated human platelets cause pulmonary hypertension and edema in isolated rabbit lungs. Role of thromboxane A2.

Macrophages, neutrophils, and platelets may play a role in acute edematous lung injury, such as that seen in the adult respiratory distress syndrome (ARDS), but their potential actions and interactions are unclear. Because stimulated human macrophages and neutrophils can release acetyl glyceryl ether phosphorylcholine (AGEPC), a potent platelet activator, we hypothesized that in ARDS, leukocyte release of AGEPC might stimulate platelets to release thromboxane A2 (TXA2), which then produces pulmonary hypertension and lung edema. In support of this premise, we found that pulmonary hypertension and edema occurred in isolated rabbit lungs perfused with human platelets and AGEPC, but not with platelets or AGEPC alone. Infusion of a vasodilator (nitroglycerin) to maintain base-line pulmonary artery pressures in lungs perfused with platelets and AGEPC prevented the development of lung edema suggesting that platelet and AGEPC-induced edema was hydrostatic in nature. Additional experiments suggested that the increased pressure was a result of TXA2 release from platelets stimulated by AGEPC. Specifically, preincubation of platelets with imidazole, a thromboxane synthetase blocker, prior to infusion with AGEPC significantly diminished pulmonary hypertension and prevented lung edema. Furthermore, pretreating lung preparations with 13-azaprostanoic acid, a TXA2 antagonist, before infusion of AGEPC and untreated platelets also reduced the pulmonary hypertension and blocked the lung edema. The role of TXA2 was further suggested when perfusates from lungs infused with platelets and AGEPC developed high levels of TXA2, whereas perfusates from controls did not. These results suggest that platelet aggregation induced by AGEPC may contribute to ARDS by releasing TXA2, which raises microvascular pressure and increases edema formation, especially when an underlying permeability defect is present.

Animals↗
PubMed1983

Controlled hyperventilation in patients with intracranial hypertension. Application and management.

When elevated intracranial pressure (ICP) complicates the course of various forms of cerebral edema, the likelihood of survival with full recovery is greatly diminished. Controlled mechanical hyperventilation effectively lowers ICP in some patients by causing cerebral vasoconstriction. Improved survival occurs in patients with elevated ICP from head trauma and intracranial infection treated with hyperventilation; however, no benefit has been demonstrated in patients with increased ICP from strokes or hypoxic brain damage. Proper management of the hyperventilation requires knowledge of basic cerebral circulatory physiology. Arterial Paco2 tensions should be maintained between 25 and 30 mm Hg. Vasoconstrictive effects of hyperventilation diminish after 48 to 72 hours when renal mechanisms compensate for the respiratory alkalosis. When hyperventilation is discontinued, the Paco2 must be gradually returned to normal values, since sudden changes may cause a marked rise in ICP.

Brain↗
PubMed1982

Massive pleural effusions from prostatic lymphangitic carcinomatosis: resolution with endocrine therapy.

Pleural effusions are a rare complication of metastatic adenocarcinoma of the prostate and have not been noted to resolve with endocrine therapy. In a patient with massive bilateral pleural effusions as the initial manifestation of underlying prostatic cancer, lung biopsy specimens documented the presence of lymphangitic carcinomatosis and pleural biopsy tissue was normal. The effusions cleared on two occasions after diethylstilbestrol diproprionate therapy was started. We conclude that massive pleural effusions occasionally complicate prostatic lymphangitic carcinomatosis and that they may resolve with endocrine therapy.

Adenocarcinoma↗
PubMed1981

Salicylate-induced pulmonary edema. Clinical features and prognosis.

To assess the course and prognosis of salicylate-induced pulmonary edema, we reviewed the records of 36 consecutive patients admitted with serum salicylate levels greater than 30 mg/dL. Pulmonary edema developed in eight patients, and pulmonary infiltrates were never seen in 28 patients. Several features distinguished the two patient groups. Persons with pulmonary edema were older, ingested salicylates chronically, and had a history of smoking. They also were more likely to present with neurologic abnormalities. proteinuria, and serum salicylate levels greater than 40 mg/dL. The severity of pulmonary edema ranged from moderate (no assisted ventilation) to severe (characteristics of adult respiratory distress syndrome requiring assisted ventilation with positive end-expiratory pressure). Pulmonary edema resolved concomitant with a decline in serum salicylate levels. We conclude that certain patients are at increased risk for salicylate pulmonary edema, which responds to measures that lower serum salicylate levels.

Adult↗
PubMed1981

Diagnosis of adult respiratory distress syndrome associated with underlying severe emphysema.

Adult respiratory distress syndrome (ARDS) notably produces bilateral homogeneous alveolar infiltrates and decreased lung compliance. We encountered a patient whose severe underlying emphysema altered these distinctive clinical features. The chest roentgenogram showed bilateral infiltrates containing multiple radiolucencies that simulated a cavitary process. Also, lung-chest wall compliances measured during mechanical ventilation were higher than usually observed in patients with ARDS. We suggest that the pathologic features of the emphysematous lung with multiple blebs and decreased elastic recoil properties impart these unique findings. When ARDS develops in a patient with severe underlying emphysema, an atypical presentation may produce a confusing clinical picture.

Humans↗
PubMed1979

Extracardiac manifestations of bacterial endocarditis.

Bacterial endocarditis is an elusive disease that challenges clinicians' diagnostic capabilities. Because it can present with various combinations of extravalvular signs and symptoms, the underlying primary disease can go unnoticed.A review of the various extracardiac manifestations of bacterial endocarditis suggests three main patterns by which the valvular infection can be obscured. (1) A major clinical event may be so dramatic that subtle evidence of endocarditis is overlooked. The rupture of a mycotic aneurysm may simulate a subarachnoid hemorrhage from a congenital aneurysm. (2) The symptoms of bacterial endocarditis may be constitutional complaints easily attributable to a routine, trivial illness. Symptoms of low-grade fever, myalgias, back pain and anorexia may mimic a viral syndrome. (3) Endocarditis poses a difficult diagnostic dilemma when it generates constellations of findings that are classic for other disorders. Complaints of arthritis and arthralgias accompanied by hematuria and antinuclear antibody may suggest systemic lupus erythematosus; a renal biopsy study showing diffuse proliferative glomerulonephritis may support this diagnosis. The combination of fever, petechiae, altered mental status, thrombocytopenia, azotemia and anemia may promote the diagnosis of thrombotic thrombocytopenic purpura. When the protean guises of bacterial endocarditis create these clinical difficulties, errors in diagnosis occur and appropriate therapy is delayed. Keen awareness of the varied disease presentations will improve success in managing endocarditis by fostering rapid diagnosis and prompt therapy.

Bone Diseases↗